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Sample records for renal sympathetic nerve

  1. Regulation of the renal sympathetic nerves in heart failure

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    Rohit eRamchandra

    2015-08-01

    Full Text Available Heart failure (HF is a serious debilitating condition with poor survival rates and an increasing level of prevalence. Heart failure is associated with an increase in renal norepinephrine spillover, which is an independent predictor of mortality in HF patients. The excessive sympatho-excitation that is a hallmark of heart failure has long-term effects that contribute to disease progression. An increase in directly recorded renal sympathetic nerve activity has also been recorded in animal models of heart failure. This review will focus on the mechanisms controlling sympathetic nerve activity to the kidney during normal conditions and alterations in these mechanisms during heart failure. In particular the roles of afferent reflexes and central mechanisms will be discussed.

  2. Eppur Si Muove: The dynamic nature of physiological control of renal blood flow by the renal sympathetic nerves.

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    Schiller, Alicia M; Pellegrino, Peter Ricci; Zucker, Irving H

    2016-08-03

    Tubuloglomerular feedback and the myogenic response are widely appreciated as important regulators of renal blood flow, but the role of the sympathetic nervous system in physiological renal blood flow control remains controversial. Where classic studies using static measures of renal blood flow failed, dynamic approaches have succeeded in demonstrating sympathetic control of renal blood flow under normal physiological conditions. This review focuses on transfer function analysis of renal pressure-flow, which leverages the physical relationship between blood pressure and flow to assess the underlying vascular control mechanisms. Studies using this approach indicate that the renal nerves are important in the rapid regulation of the renal vasculature. Animals with intact renal innervation show a sympathetic signature in the frequency range associated with sympathetic vasomotion that is eliminated by renal denervation. In conscious rabbits, this sympathetic signature exerts vasoconstrictive, baroreflex control of renal vascular conductance, matching well with the rhythmic, baroreflex-influenced control of renal sympathetic nerve activity and complementing findings from other studies employing dynamic approaches to study renal sympathetic vascular control. In this light, classic studies reporting that nerve stimulation and renal denervation do not affect static measures of renal blood flow provide evidence for the strength of renal autoregulation rather than evidence against physiological renal sympathetic control of renal blood flow. Thus, alongside tubuloglomerular feedback and the myogenic response, renal sympathetic outflow should be considered an important physiological regulator of renal blood flow. Clinically, renal sympathetic vasomotion may be important for solving the problems facing the field of therapeutic renal denervation.

  3. Effects of renal sympathetic nerve radiofrequency ablation on norepinephrine spillover rate and sympathetic nerve activity in dogs with hypertension

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    Hang YU

    2012-11-01

    Full Text Available Objective  To evaluate the validity and explore the mechanism of renal sympathetic denervation (RSD in the treatment of dogs with hypertension reproduced by constriction of abdominal aorta. Methods  The hypertension model was reproduced by constriction of abdominal aorta in 20 adult healthy dogs. These dogs were then randomly divided into the treatment group and control group (10 each. Renal sympathetic nerve radiofrequency ablation was done in treatment group 1 month after modeling. The foreleg blood pressure, sympathetic activity and norepinephrine overflow rate of dogs in two groups were detected before modeling, and 1, 2 and 3 months after modeling, and the trend of the change was also observed. Results  One month after modeling, the systolic blood pressure (SBP, diastolic blood pressure (DBP and mean arterial blood pressure (MAP were elevated significantly in control group (146.7±21.0, 89.0±12.7 and 108.3±14.9mmHg compared with those before modeling (119.5±13.2, 76.5±7.8 and 90.9±8mmHg, P < 0.05. The renal sympathetic activity impulse and norepinephrine spillover rate were also enhanced significantly (P < 0.05. The renal sympathetic nerve activity obviously decreased in the treatment group after the operation, and then increased 2 months after the ablation. The norepinephrine spillover rate in treatment group increased significantly 1 month after modeling (P < 0.05, and decreased after ablation, and it lasted to the end of the experiment (P < 0.05. One and two months after ablation, the norepinephrine spillover rate was lower in treatment group than in control group (P < 0.05. Conclusion  Renal sympathetic nerve radiofrequency ablation significantly inhibits the elevation of norepinephrine spillover rate and sympathetic nerve activity in dogs with hypertension.

  4. Renal sympathetic nerve activity during asphyxia in fetal sheep.

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    Booth, Lindsea C; Malpas, Simon C; Barrett, Carolyn J; Guild, Sarah-Jane; Gunn, Alistair J; Bennet, Laura

    2012-07-01

    The sympathetic nervous system (SNS) is an important mediator of fetal adaptation to life-threatening in utero challenges, such as asphyxia. Although the SNS is active well before term, SNS responses mature significantly over the last third of gestation, and its functional contribution to adaptation to asphyxia over this critical period of life remains unclear. Therefore, we examined the hypotheses that increased renal sympathetic nerve activity (RSNA) is the primary mediator of decreased renal vascular conductance (RVC) during complete umbilical cord occlusion in preterm fetal sheep (101 ± 1 days; term 147 days) and that near-term fetuses (119 ± 0 days) would have a more rapid initial vasomotor response, with a greater increase in RSNA. Causality of the relationship of RSNA and RVC was investigated using surgical (preterm) and chemical (near-term) denervation. All fetal sheep showed a significant increase in RSNA with occlusion, which was more sustained but not significantly greater near-term. The initial fall in RVC was more rapid in near-term than preterm fetal sheep and preceded the large increase in RSNA. These data suggest that although RSNA can increase as early as 0.7 gestation, it is not the primary determinant of RVC. This finding was supported by denervation studies. Interestingly, chemical denervation in near-term fetal sheep was associated with an initial fall in blood pressure, suggesting that by 0.8 gestation sympathetic innervation of nonrenal vascular beds is critical to maintain arterial blood pressure during the rapid initial adaptation to asphyxia.

  5. [Role of renal sympathetic nerve and oxidative stress in foot shock-induced hypertension in rats].

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    Jiang, Ren-Di; Zhang, Zhe; Xu, Jian-Bing; Dong, Tao; Zhang, Guo-Xing

    2015-06-25

    The present study was aimed to investigate the roles of renal sympathetic nerve and oxidative stress in the development of foot shock-induced hypertension. Ninety rats were divided into 6 groups (the number of each group was 15): control group, foot shock group, denervation of renal sympathetic nerve group, denervation of renal sympathetic nerve + foot shock group, Tempol treatment + foot shock group, denervation of renal sympathetic nerve + Tempol treatment + foot shock group. Rats were received electrical foot shock for 14 days (2-4 mA, 75 V, shocks of 50-100 ms every 30 s, for 4 h each session through an electrified grid floor every day). Renal sympathetic ablation was used to remove bilateral renal sympathetic nerve in rats (rats were allowed to recover for one week before the beginning of the foot shock procedure). The antioxidant Tempol was injected intraperitoneally at 1 h before foot shock. Systolic blood pressure was measured at 1 h after foot shock on day 0, 3, 7, 10 and 14. Contents of thiobarbituric acid reactive substance (TBARS), renin, angiotensin II (AngII) and glutathione peroxidase (GSH-Px) in plasma were measured by ELISA after 14-day foot shock. The results showed that systolic blood pressure of foot shock group was significantly increased (P indirectly activate renin-angiotensin-aldosterone system, so the foot shock-induced high blood pressure may be maintained and hypertension may therefore be produced.

  6. Effect of percutaneous renal sympathetic nerve radiofrequency ablation in patients with severe heart failure.

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    Dai, Qiming; Lu, Jing; Wang, Benwen; Ma, Genshan

    2015-01-01

    This study aimed to investigate the clinical feasibility and effects of percutaneous renal sympathetic nerve radiofrequency ablation in patients with heart failure. A total of 20 patients with heart failure were enrolled, aged from 47 to 75 years (63±10 years). They were divided into the standard therapy (n = 10), and renal nerve radiofrequency ablation groups (n = 10). There were 15 males and 5 female patients, including 8 ischemic cardiomyopathy, 8 dilated cardiomyopathy, and 8 hypertensive cardiopathy. All of the patients met the criteria of New York Heart Association classes III-IV cardiac function. Patients with diabetes and renal failure were excluded. Percutaneous renal sympathetic nerve radiofrequency ablation was performed on the renal artery wall under X-ray guidance. Serum electrolytes, neurohormones, and 24 h urine volume were recorded 24 h before and after the operation. Echocardiograms were performed to obtain left ventricular ejection fraction at baseline and 6 months. Heart rate, blood pressure, symptoms of dyspnea and edema were also monitored. After renal nerve ablation, 24 h urine volume was increased, while neurohormone levels were decreased compared with those of pre-operation and standard therapy. No obvious change in heart rate or blood pressure was recorded. Symptoms of heart failure were improved in patients after the operation. No complications were recorded in the study. Percutaneous renal sympathetic nerve radiofrequency ablation may be a feasible, safe, and effective treatment for the patients with severe congestive heart failure.

  7. Direct conscious telemetry recordings demonstrate increased renal sympathetic nerve activity in rats with chronic kidney disease

    OpenAIRE

    Ibrahim M. Salman; Divya Sarma Kandukuri; Joanne Lesley Harrison; Cara Margaret Hildreth; Jacqueline Kathleen Phillips

    2015-01-01

    Chronic kidney disease (CKD) is associated with sympathetic hyperactivity and impaired blood pressure control reflex responses, yet direct evidence demonstrating these features of autonomic dysfunction in conscious animals is still lacking. Here we measured renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) using telemetry-based recordings in a rat model of CKD, the Lewis Polycystic Kidney (LPK) rat, and assessed responses to chemoreflex activation and acute stress. Male...

  8. EFFECTS OF INTRAVENOUS FENTANYL ON SPONTANEOUS RENAL SYMPATHETIC NERVE ACTIVITY IN NORMAL AND VAGOTOMIZED RABBITS

    Institute of Scientific and Technical Information of China (English)

    Chen Wang; James G.Whitwam

    2004-01-01

    Objective To investigate the roles of sympathetic and vagus nerves in hypotension and bradycardia induced by fentanyl.Methods Fourteen rabbits were divided into 2 groups: normal and vagotomized rabbits. Rabbits were anesthetized,paralyzed, and artificial ventilated. Right renal sympathetic nerve was exposed and prepared for recording electrical activity.Fentanyl was injected intravenously in incremental doses of 1, 4, 15, 30, and 50 μg/kg at 10 minutes intervals.Results Fentanyl significantly reduced the spontaneous activity of renal sympathetic nerve, mean arterial pressure, and heart rate above a total dose of 20 μg/kg in both normal and vagotomized rabbits. However, normal rabbits spontaneous sympathetic nerve activity and mean arterial pressure were more depressed than vagotomized rabbits at total doses of 50 and 100 μg/kg. There were no significant difference in the reduction of heart rate between normal and vagotomized rabbits.Conclusion Fentanyl induction of bradycardia and hypotension in rabbits is mainly due to depression of sympathetic nerve activity.

  9. Thin-fiber mechanoreceptors reflexly increase renal sympathetic nerve activity during static contraction.

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    Kim, Jong Kyung; Hayes, Shawn G; Kindig, Angela E; Kaufman, Marc P

    2007-02-01

    The renal vasoconstriction induced by the sympathetic outflow during exercise serves to direct blood flow from the kidney toward the exercising muscles. The renal circulation seems to be particularly important in this regard, because it receives a substantial part of the cardiac output, which in resting humans has been estimated to be 20%. The role of group III mechanoreceptors in causing the reflex renal sympathetic response to static contraction remains an open question. To shed some light on this question, we recorded the renal sympathetic nerve responses to static contraction before and after injection of gadolinium into the arterial supply of the statically contracting triceps surae muscles of decerebrate unanesthetized and chloralose-anesthetized cats. Gadolinium has been shown to be a selective blocker of mechanogated channels in thin-fiber muscle afferents, which comprise the afferent arm of the exercise pressor reflex arc. In decerebrate (n = 15) and chloralose-anesthetized (n = 12) cats, we found that gadolinium (10 mM; 1 ml) significantly attenuated the renal sympathetic nerve and pressor responses to static contraction (60 s) after a latent period of 60 min; both responses recovered after a latent period of 120 min. We conclude that thin-fiber mechanoreceptors supplying contracting muscle are involved in some of the renal vasoconstriction evoked by the exercise pressor reflex.

  10. Sympathetic nerve-derived ATP regulates renal medullary blood flow via vasa recta pericytes

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    Scott S Wildman

    2013-10-01

    Full Text Available Pericyte cells are now known to be a novel locus of blood flow control, being able to regulate capillary diameter via their unique morphology and expression of contractile proteins. We have previously shown that exogenous ATP causes constriction of vasa recta via renal pericytes, acting at a variety of membrane bound P2 receptors on descending vasa recta, and therefore may be able to regulate medullary blood flow (MBF. Regulation of MBF is essential for appropriate urine concentration and providing essential oxygen and nutrients to this region of high, and variable, metabolic demand. Various sources of endogenous ATP have been proposed, including from epithelial, endothelial and red blood cells in response to stimuli such as mechanical stimulation, local acidosis, hypoxia, and exposure to various hormones. Extensive sympathetic innervation of the nephron has previously been shown, however the innervation reported has focused around the proximal and distal tubules, and ascending loop of Henle. We hypothesise that sympathetic nerves are an additional source of ATP acting at renal pericytes and therefore regulate MBF. Using a rat live kidney slice model in combination with video imaging and confocal microscopy techniques we firstly show sympathetic nerves in close proximity to vasa recta pericytes in both the outer and inner medulla. Secondly, we demonstrate pharmacological stimulation of sympathetic nerves in situ (by tyramine evokes pericyte-mediated vasoconstriction of vasa recta capillaries; inhibited by the application of the P2 receptor antagonist suramin. Lastly, tyramine-evoked vasoconstriction of vasa recta by pericytes is significantly less than ATP-evoked vasoconstriction. Sympathetic innervation may provide an additional level of functional regulation in the renal medulla that is highly localized. It now needs to be determined under which physiological/pathophysiological circumstances that sympathetic innervation of renal pericytes is

  11. Leptin into the rostral ventral lateral medulla (RVLM augments renal sympathetic nerve activity and blood pressure

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    Maria J Barnes

    2014-08-01

    Full Text Available Leptin is a hormone released from adipose tissue. While this hormone normally acts to reduce feeding behavior and increase energy expenditure, in obesity, resistance to these effects occurs even though the hormone is released in large amounts. Although leptin no longer works to suppress feeding in the obese, leptin retains its potent effects on other autonomic functions such as blood pressure regulation. Leptin has been associated with hypertension and increased sympathetic autonomic activity. Therefore, leptin is emerging as a major contributor to the hypertensive state observed in obesity. Sympathetic control of blood pressure is maintained principally by autonomic reflex control circuits in the caudal brainstem. The rostral ventral-lateral medulla (RVLM is the primary regulator of the sympathetic nervous system, sending excitatory fibers to sympathetic preganglionic neurons to regulate sympathetic control over resistance vessels and blood pressure. Previous studies from our laboratory have shown that neurons in the ventral lateral medulla express leptin receptors (ObRb. Our present study using pseudo-rabies multi-synaptic retrograde tract tracing and immunohistochemical methods revealed that neurons within the RVLM that send sympathetic projections to the kidney express leptin receptors. Acute microinjection of leptin (1 and 3µg; 40nL into the RVLM evoked a significant increase in Mean Arterial Pressure (MAP and renal sympathetic nerve activity (RSNA. When the 3µg dose of leptin was preceded with a leptin antagonist, (SLAN-4; 1ng, it attenuated the cardiovascular response of leptin. Taken together, these data suggest that leptin’s actions within the RVLM may influence blood pressure and renal sympathetic nerve activity.

  12. [Sympathetic nerve activity in chronic renal failure - what are the therapeutic options?].

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    Hausberg, M; Tokmak, F

    2013-11-01

    Patients with chronic renal failure are characterized by a tonic elevation of sympathetic tone. This factor largely contributes to their increased cardiovascular risk. The increased sympathetic drive is caused by activiation of renal afferent fibers in the diseased kidneys. Therapeutic options for hypertensive patients with chronic renal failure with respect to their sympathetic overactivity are inhibitors of the renin-angiotensin-system and central sympatholytic drugs. The role of catheter-based renal denervation in these patients is currently under investigation.

  13. Direct conscious telemetry recordings demonstrate increased renal sympathetic nerve activity in rats with chronic kidney disease.

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    Salman, Ibrahim M; Sarma Kandukuri, Divya; Harrison, Joanne L; Hildreth, Cara M; Phillips, Jacqueline K

    2015-01-01

    Chronic kidney disease (CKD) is associated with sympathetic hyperactivity and impaired blood pressure control reflex responses, yet direct evidence demonstrating these features of autonomic dysfunction in conscious animals is still lacking. Here we measured renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) using telemetry-based recordings in a rat model of CKD, the Lewis Polycystic Kidney (LPK) rat, and assessed responses to chemoreflex activation and acute stress. Male LPK and Lewis control animals (total n = 16) were instrumented for telemetric recording of RSNA and MAP. At 12-13 weeks-of-age, resting RSNA and MAP, sympathetic and haemodynamic responses to both peripheral (hypoxia: 10% O2) and central chemoreflex (hypercapnia: 7% CO2) activation and acute stress (open-field exposure), were measured. As indicators of renal function, urinary protein (UPro) and creatinine (UCr) levels were assessed. LPK rats had higher resting RSNA (1.2 ± 0.1 vs. 0.6 ± 0.1 μV, p dual conscious telemetry recording of RSNA and MAP in a genetic rodent model of CKD. Elevated RSNA is likely a key contributor to the marked hypertension in this model, while attenuated RSNA and MAP responses to central chemoreflex activation and acute stress in the LPK indicate possible deficits in the neural processing of autonomic outflows evoked by these sympathoexcitatory pathways.

  14. Direct conscious telemetry recordings demonstrate increased renal sympathetic nerve activity in rats with chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Ibrahim M Salman

    2015-08-01

    Full Text Available Chronic kidney disease (CKD is associated with sympathetic hyperactivity and impaired blood pressure control reflex responses, yet direct evidence demonstrating these features of autonomic dysfunction in conscious animals is still lacking. Here we measured renal sympathetic nerve activity (RSNA and mean arterial pressure (MAP using telemetry-based recordings in a rat model of CKD, the Lewis Polycystic Kidney (LPK rat, and assessed responses to chemoreflex activation and acute stress. Male LPK and Lewis control animals (total n=16 were instrumented for telemetric recording of RSNA and MAP. At 12–13 weeks-of-age, resting RSNA and MAP, sympathetic and haemodynamic responses to both peripheral (hypoxia: 10% O2 and central chemoreflex (hypercapnia: 7% CO2 activation and acute stress (open-field exposure, were measured. As indicators of renal function, urinary protein (UPro and creatinine (Ucr levels were assessed. LPK rats had higher resting RSNA (1.2±0.1 vs. 0.6±0.1 µV, p<0.05 and MAP (151±8 vs. 97±2 mmHg, p<0.05 compared to Lewis. MAP was negatively correlated with Ucr (r=-0.80, p=0.002 and positively correlated with RSNA (r=0.66, p=0.014, with multiple linear regression modeling indicating the strongest correlation was with Ucr. RSNA and MAP responses to activation of the central chemoreflex and open-field stress were reduced in the LPK relative to the Lewis (all p<0.05. This is the first description of dual conscious telemetry recording of RSNA and MAP in a genetic rodent model of CKD. Elevated RSNA is likely a key contributor to the marked hypertension in this model, while attenuated RSNA and MAP responses to central chemoreflex activation and acute stress in the LPK indicate possible deficits in the neural processing of autonomic outflows evoked by these sympathoexcitatory pathways.

  15. Modelling of the dynamic relationship between arterial pressure, renal sympathetic nerve activity and renal blood flow in conscious rabbits.

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    Berger, C S; Malpas, S C

    1998-12-01

    A linear autoregressive/moving-average model was developed to describe the dynamic relationship between mean arterial pressure (MAP), renal sympathetic nerve activity (SNA) and renal blood flow (RBF) in conscious rabbits. The RBF and SNA to the same kidney were measured under resting conditions in a group of eight rabbits. Spectral analysis of the data sampled at 0.4 Hz showed that the low-pass bandwidth of the signal power for RBF was approximately 0. 05 Hz. An autoregressive/moving-average model with an exogenous input (ARMAX) was then derived (using the iterative Gauss-Newton algorithm provided by the MATLAB identification Toolbox), with MAP and SNA as inputs and RBF as output, to model the low-frequency fluctuations. The model step responses of RBF to changes in SNA and arterial pressure indicated an overdamped response with a settling time that was usually less than 2 s. Calculated residuals from the model indicated that 79 5 % (mean s.d., averaged over eight independent experiments) of the variation in RBF could be accounted for by the variations in arterial pressure and SNA. Two additional single-input models for each of the inputs were similarly obtained and showed conclusively that changes in RBF, in the conscious resting rabbit, are a function of both SNA and MAP and that the SNA signal has the predominant effect. These results indicate a strong reliance on SNA for the dynamic regulation of RBF. Such information is likely to be important in understanding the diminished renal function that occurs in a variety of disease conditions in which overactivity of the sympathetic nervous system occurs.

  16. Baroreflex control of renal sympathetic nerve activity and heart rate in near-term fetal sheep.

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    Booth, Lindsea C; Gunn, Alistair J; Malpas, Simon C; Barrett, Carolyn J; Davidson, Joanne O; Guild, Sarah-Jane; Bennet, Laura

    2011-08-01

    Late preterm infants, born between 34 and 36 weeks gestation, have significantly higher morbidity than neonates born at full term, which may be partly related to reduced sensitivity of the arterial baroreflex. The present study assessed baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) in near-term fetal sheep at 123 ± 1 days gestation. At this age, although fetuses are not fully mature in some respects (term is 147 days), sleep-state cycling is established [between high-voltage, low-frequency (HV) and low-voltage, high-frequency (LV) sleep], and neural myelination is similar to the term human infant. Fetal sheep were instrumented to record blood pressure (BP), HR (n = 15) and RSNA (n = 5). Blood pressure was manipulated using vasoactive drugs, phenylephrine and sodium nitroprusside. In both HV and LV sleep, phenylephrine was associated with increased arterial BP and decreased HR. In HV sleep, phenylephrine was associated with a fall in RSNA, from 124 ± 14 to 58 ± 11% (P fall in BP after sodium nitroprusside was associated with a significant increase in HR during LV but not HV sleep, and there was no significant effect of hypotension on RSNA. These data demonstrate that in near-term fetal sheep baroreflex activity is only partly active and is highly modulated by sleep state. Critically, there was no RSNA response to marked hypotension; this finding has implications for the ability of the late preterm fetus to adapt to low BP.

  17. Perfusion of isolated carotid sinus with hydrogen sulfide attenuated the renal sympathetic nerve activity in anesthetized male rats.

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    Guo, Q; Wu, Y; Xue, H; Xiao, L; Jin, S; Wang, R

    2016-07-18

    The purpose of the present study was to define the indirect central effect of hydrogen sulfide (H(2)S) on baroreflex control of sympathetic outflow. Perfusing the isolated carotid sinus with sodium hydrosulfide (NaHS), a H(2)S donor, the effect of H(2)S was measured by recording changes of renal sympathetic nerve activity (RSNA) in anesthetized male rats. Perfusion of isolated carotid sinus with NaHS (25, 50, 100 micromol/l) dose and time-dependently inhibited sympathetic outflow. Preconditioning of glibenclamide (20 micromol/l), a ATP-sensitive K(+) channels (K(ATP)) blocker, the above effect of NaHS was removed. With 1, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-[trifluoromethyl] phenyl) pyridine-3-carboxylic acid methyl ester (Bay K8644, 500 nmol/l) pretreatment, which is an agonist of L-calcium channels, the effect of NaHS was eliminated. Perfusion of cystathionine gamma-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 micromol/l), increased sympathetic outflow. The results show that exogenous H(2)S in the carotid sinus inhibits sympathetic outflow. The effect of H(2)S is attributed to opening K(ATP) channels and closing the L-calcium channels.

  18. Arterial baroreceptor reflex control of renal sympathetic nerve activity following chronic myocardial infarction in male, female, and ovariectomized female rats.

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    Pinkham, Maximilian I; Whalley, Gillian A; Guild, Sarah-Jane; Malpas, Simon C; Barrett, Carolyn J

    2015-07-15

    There is controversy regarding whether the arterial baroreflex control of renal sympathetic nerve activity (SNA) in heart failure is altered. We investigated the impact of sex and ovarian hormones on changes in the arterial baroreflex control of renal SNA following a chronic myocardial infarction (MI). Renal SNA and arterial pressure were recorded in chloralose-urethane anesthetized male, female, and ovariectomized female (OVX) Wistar rats 6-7 wk postsham or MI surgery. Animals were grouped according to MI size (sham, small and large MI). Ovary-intact females had a lower mortality rate post-MI (24%) compared with both males (38%) and OVX (50%) (P renal SNA. As a result, the male large MI group (49 ± 6 vs. 84 ± 5% in male sham group) and OVX large MI group (37 ± 3 vs. 75 ± 5% in OVX sham group) displayed significantly reduced arterial baroreflex range of control of normalized renal SNA (P renal SNA was unchanged regardless of MI size. In males and OVX there was a significant, positive correlation between left ventricle (LV) ejection fraction and arterial baroreflex range of control of normalized renal SNA, but not absolute renal SNA, that was not evident in ovary-intact females. The current findings demonstrate that the arterial baroreflex control of renal SNA post-MI is preserved in ovary-intact females, and the state of left ventricular dysfunction significantly impacts on the changes in the arterial baroreflex post-MI.

  19. Activation of NTS A2a adenosine receptors differentially resets baroreflex control of renal vs. adrenal sympathetic nerve activity.

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    Ichinose, Tomoko K; O'Leary, Donal S; Scislo, Tadeusz J

    2009-04-01

    The role of nucleus of solitary tract (NTS) A(2a) adenosine receptors in baroreflex mechanisms is controversial. Stimulation of these receptors releases glutamate within the NTS and elicits baroreflex-like decreases in mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas inhibition of these receptors attenuates HR baroreflex responses. In contrast, stimulation of NTS A(2a) adenosine receptors increases preganglionic adrenal sympathetic nerve activity (pre-ASNA), and the depressor and sympathoinhibitory responses are not markedly affected by sinoaortic denervation and blockade of NTS glutamatergic transmission. To elucidate the role of NTS A(2a) adenosine receptors in baroreflex function, we compared full baroreflex stimulus-response curves for HR, RSNA, and pre-ASNA (intravenous nitroprusside/phenylephrine) before and after bilateral NTS microinjections of selective adenosine A(2a) receptor agonist (CGS-21680; 2.0, 20 pmol/50 nl), selective A(2a) receptor antagonist (ZM-241385; 40 pmol/100 nl), and nonselective A(1) + A(2a) receptor antagonist (8-SPT; 1 nmol/100 nl) in urethane/alpha-chloralose anesthetized rats. Activation of A(2a) receptors decreased the range, upper plateau, and gain of baroreflex-response curves for RSNA, whereas these parameters all increased for pre-ASNA, consistent with direct effects of the agonist on regional sympathetic activity. However, no resetting of baroreflex-response curves along the MAP axis occurred despite the marked decreases in baseline MAP. The antagonists had no marked effects on baseline variables or baroreflex-response functions. We conclude that the activation of NTS A(2a) adenosine receptors differentially alters baroreflex control of HR, RSNA, and pre-ASNA mostly via non-baroreflex mechanism(s), and these receptors have virtually no tonic action on baroreflex control of these sympathetic outputs.

  20. Renal Sympathetic Denervation: Hibernation or Resurrection?

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    Papademetriou, Vasilios; Doumas, Michael; Tsioufis, Costas

    2016-01-01

    The most current versions of renal sympathetic denervation have been invented as minimally invasive approaches for the management of drug-resistant hypertension. The anatomy, physiology and pathophysiology of renal sympathetic innervation provide a strong background supporting an important role of the renal nerves in the regulation of blood pressure (BP) and volume. In addition, historical data with surgical sympathectomy and experimental data with surgical renal denervation indicate a beneficial effect on BP levels. Early clinical studies with transcatheter radiofrequency ablation demonstrated impressive BP reduction, accompanied by beneficial effects in target organ damage and other disease conditions characterized by sympathetic overactivity. However, the failure of the SYMPLICITY 3 trial to meet its primary efficacy end point raised a lot of concerns and put the field of renal denervation into hibernation. This review aims to translate basic research into clinical practice by presenting the anatomical and physiological basis for renal sympathetic denervation, critically discussing the past and present knowledge in this field, where we stand now, and also speculating about the future of the intervention and potential directions for research. © 2016 S. Karger AG, Basel.

  1. Central Administration of Insulin and Leptin Together Enhance Renal Sympathetic Nerve Activity and Fos Production in the Arcuate Nucleus

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    Habeeballah, Hamza; Alsuhaymi, Naif; Stebbing, Martin J.; Jenkins, Trisha A.; Badoer, Emilio

    2017-01-01

    There is considerable interest in the central actions of insulin and leptin. Both induce sympatho-excitation. This study (i) investigated whether centrally administered leptin and insulin together elicits greater increases in renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) than when given alone, and (ii) quantified the number of activated neurons in brain regions influencing SNA, to identify potential central sites of interaction. In anesthetised (urethane 1.4–1.6 g/kg iv) male Sprague-Dawley rats, RSNA, MAP, and HR were recorded following intracerebroventricular (ICV) saline (control; n = 5), leptin (7 μg; n = 5), insulin (500 mU; n = 4) and the combination of leptin and insulin; (n = 4). Following leptin or insulin alone, RSNA was significantly increased (74 and 62% respectively). MAP responses were not significantly different between the groups. Insulin alone significantly increased HR. Leptin alone also increased HR but it was significantly less than following insulin alone (P < 0.005). When leptin and insulin were combined, the RSNA increase (124%) was significantly greater than the response to either alone. There were no differences between the groups in MAP responses, however, the increase in HR induced by insulin was attenuated by leptin. Of the brain regions examined, only in the arcuate nucleus did leptin and insulin together increase the number of Fos-positive cell nuclei significantly more than leptin or insulin alone. In the lamina terminalis and rostroventrolateral medulla, leptin and insulin together increased Fos, but the effect was not greater than leptin alone. The results suggest that when central leptin and insulin levels are elevated, the sympatho-excitatory response in RSNA will be greater. The arcuate nucleus may be a common site of cardiovascular integration. PMID:28119622

  2. Sympathetic nervous system and chronic renal failure.

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    Boero, R; Pignataro, A; Ferro, M; Quarello, F

    2001-01-01

    The aim of this work was to review evidence on the role of the sympathetic nervous system (SNS) in chronic renal failure (CRF). Three main points are discussed: 1) SNS and pathogenesis of arterial hypertension; 2) SNS and cardiovascular risk; 3) implication of SNS in arterial hypotension during hemodialysis. Several lines of evidence indicate the presence of a sympathetic hyperactivity in CRF, and its relationship with arterial hypertension. It is suggested that diseased kidneys send afferent nervous signals to central integrative sympathetic nuclei, thus contributing to the development and maintenance of arterial hypertension. The elimination of these impulses with nephrectomy could explain the concomitant reduction of blood pressure. Several experiments confirmed this hypothesis. Regarding SNS and cardiovascular risk, some data suggest that reduced heart rate variability identifies an increased risk for both all causes and sudden death, independently from other recognized risk factors. Symptomatic hypotension is a common problem during hemodialysis treatment, occurring in approximately 20-30% of all hemodialysis sessions and is accompanied by acute withdrawal of sympathetic activity, vasodilation and relative bradicardia. This reflex is thought to be evoked by vigorous contraction of a progressively empty left ventricle, activating cardiac mechanoceptors. This inhibits cardiovascular centers through vagal afferents, and overrides the stimulation by baroreceptor deactivation. Alternative explanations include cerebral ischemia and increased production of nitric oxide, which inhibit central sympathetic activity. It is hoped that therapies aimed at modulating sympathetic nerve activity in patients with CRF will ameliorate their prognosis and quality of life.

  3. Sympathetic vasoconstrictor nerve function in alcoholic neuropathy

    DEFF Research Database (Denmark)

    Jensen, K; Andersen, K; Smith, T;

    1984-01-01

    The peripheral sympathetic vasomotor nerve function was investigated in 18 male chronic alcoholics admitted for intellectual impairment or polyneuropathy. By means of the local 133Xenon washout technique, the sympathetic veno-arteriolar axon-reflex was studied. This normally is responsible for a ...

  4. Renal sympathetic denervation: MDCT evaluation of the renal arteries.

    LENUS (Irish Health Repository)

    Hutchinson, Barry D

    2013-08-01

    Percutaneous transluminal renal sympathetic denervation is a new treatment of refractory systemic hypertension. The purpose of this study was to assess the clinical utility of MDCT to evaluate the anatomic configuration of the renal arteries in the context of renal sympathetic denervation.

  5. Clinical research progress in percutaneous catheter ablation of renal sympathetic nerve%经导管肾交感神经射频消融术临床研究进展

    Institute of Scientific and Technical Information of China (English)

    潘涛; 郭金和; 滕皋军

    2015-01-01

    Transcatheter renal sympathetic denervation with radiofrequency ablation has become a new treatment for refractory hypertension.Recent studies have showed that renal sympathetic denervation can also treat the diseases that are related to increased sympathetic nerve activity, such as metabolic diseases, cardiac disfunction, arrhythmia, obstructive sleep apnea syndrome, polycystic ovary syndrome, renal failure, etc. This paper aims to make a general review on the recent clinical research progress about renal sympathetic denervation with radiofrequency ablation.%经导管肾交感神经射频消融术(RDN)是治疗顽固性高血压的新手段,进一步研究发现RDN术还可治疗交感神经活性增高相关疾病,如代谢性疾病、心功能不全、心律失常、阻塞性睡眠呼吸暂停综合征、多囊卵巢综合征和肾功能不全等.本文就RDN术临床研究进展作一综述.

  6. Effects of leptin on sympathetic nerve activity in conscious mice.

    Science.gov (United States)

    Morgan, Donald A; Despas, Fabien; Rahmouni, Kamal

    2015-09-01

    The adipocyte-derived hormone, leptin, has emerged as an important regulator of regional sympathetic nerve activity (SNA) with pathophysiological implications in obesity. Genetically engineered mice are useful to understand the molecular pathways underlying the SNA responses evoked by leptin. However, so far the effect of leptin on direct SNA in mice has been studied under general anesthesia. Here, we examined the sympathetic responses evoked by leptin in conscious mice. Mice were instrumented, under ketamine/xylazine anesthesia, with renal or lumbar SNA recordings using a thin (40 gauge) bipolar platinum-iridium wire. The electrodes were exteriorized at the nape of the neck and mice were allowed (5 h) to recover from anesthesia. Interestingly, the reflex increases in renal and lumbar SNA caused by sodium nitroprusside (SNP)-induced hypotension was higher in the conscious phase versus the anesthetized state, whereas the increase in both renal and lumbar SNA evoked by leptin did not differ between anesthetized or conscious mice. Next, we assessed whether isoflurane anesthesia would yield a better outcome. Again, the SNP-induced increase in renal SNA and baroreceptor-renal SNA reflex were significantly elevated in the conscious states relative to isoflurane-anesthetized phase, but the renal SNA response induced by leptin in the conscious states were qualitatively comparable to those evoked above. Thus, despite improvement in sympathetic reflexes in conscious mice the sympathetic responses evoked by leptin mimic those induced during anesthesia. © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

  7. New treatment for old disease: management of resistant hypertension by percutaneous renal sympathetic denervation.

    Science.gov (United States)

    Kanai, Takashi; Krum, Henry

    2013-09-01

    Hypertension is a major contributor to cardiovascular events, such as stroke and myocardial infarction, with accelerated sympathetic nerve activity implicated in its pathogenesis. However, hypertension in many patients is not adequately controlled, despite the availability of numerous medication classes. Novel procedure-as well as device-based strategies, such as percutaneous renal sympathetic nerve denervation therapy-have been developed to improve blood pressure in these refractory patients. Renal sympathetic denervation delivers not only a decrease in blood pressure levels but also renal as well as systemic sympathetic nerve activity. The reduction in blood pressure appears to be sustained over 3 years after the procedure, which implies no counterregulatory mechanism or re-innervation of afferent renal sympathetic nerve so far. Renal sympathetic denervation is expected to be a promising treatment for patients with hypertension, congestive heart failure, chronic kidney disease, and metabolic syndrome implicated in the pathogenesis of potentiated sympathetic nerve activity. This review will focus on the current devices and procedures, their outcomes and prospects in the treatment of hypertension.

  8. Renal sympathetic nervous system and the effects of denervation on renal arteries

    Institute of Scientific and Technical Information of China (English)

    Arun; Kannan; Raul; Ivan; Medina; Nagapradeep; Nagajothi; Saravanan; Balamuthusamy

    2014-01-01

    Resistant hypertension is associated with chronic activation of the sympathetic nervous system resulting in various comorbidities. The prevalence of resistant hypertension is often under estimated due to various reasons. Activation of sympathetic nervous system at the renal-as well as systemic-level contributes to the increased level of catecholamines and resulting increase in the blood pressure. This increased activity was demonstrated by increased muscle sympathetic nerve activity and renal and total body noradrenaline spillover. Apart from the hypertension, it is hypothesized to be associated with insulin resistance, congestive heart failure and obstructive sleep apnea. Renal denervation is a novel procedure where the sympathetic afferent and efferent activity is reduced by various techniques and has been used successfully to treat drug-resistant hypertension improvement of various metabolic derangements.Renal denervation has the unique advantage of offering the denervation at the renal level, thus mitigating the systemic side effects. Renal denervation can be done by various techniques including radiofrequency ablation, ultrasound guided ablation and chemical ablation. Various trials evaluated the role of renal denervation in the management of resistant hypertension and have found promising results. More studies are underway to evaluate the role of renal denervation in patients presenting with resistant hypertension in different scenarios. Appropriate patient selection might be the key in determining the effectiveness of the procedure.

  9. Effects of renal sympathetic nerve radiofrequency ablation on norepinephrine spillover rate and sympathetic nerve activity in dogs with hypertension%肾交感神经射频消融术对高血压犬去甲肾上腺素溢出率及交感神经活性的影响

    Institute of Scientific and Technical Information of China (English)

    余航; 杨成明; 李慧杰; 曾春雨; 方玉强; 何多芬; 张小群; 温春兰

    2012-01-01

    目的 评价肾交感神经射频消融术(RSD)治疗腹主动脉缩窄型高血压犬的有效性和作用机制.方法 成年健康杂种犬20只,采用腹主动脉缩窄法建立高血压模型.模型建立后,随机分为治疗组(n=10)和对照组(n=10).治疗组犬于建模后1个月行双侧肾交感神经射频消融术.分别于建立模型前和建立模型后1、2、3个月,测定犬前上臂血压、交感神经活性及去甲肾上腺素溢出率并观察其变化趋势.结果 建模后1个月,对照组前上臂收缩压(SBP)、舒张压(DBP)和平均动脉压(MAP)与建模前比较均明显升高(P<0.05),肾交感神经活性冲动明显增强,去甲肾上腺素溢出率水平明显增高(P<0.05).治疗组RSD手术即刻肾交感神经活性明显下降,至消融后2个月略有增高;去甲肾上腺素溢出率水平在建模后1个月显著增高(P<0.05),消融后显著降低并一直持续至实验结束(P<0.05).与对照组比较,治疗组消融后1个月、2个月去甲肾上腺素溢出率水平显著降低(P<0.05).结论 RSD对于高血压犬去甲肾上腺素溢出率及交感神经活性均有明显抑制作用.%Objective To evaluate the validity and explore the mechanism of renal sympathetic denervation (RSD) in the treatment of dogs with hypertension reproduced by constriction of abdominal aorta. Methods The hypertension model was reproduced by constriction of abdominal aorta in 20 adult healthy dogs. These dogs were then randomly divided into the treatment group and control group (10 each). Renal sympathetic nerve radiofrequency ablation was done in treatment group 1 month after modeling. The foreleg blood pressure, sympathetic activity and norepinephrine overflow rate of dogs in two groups were detected before modeling, and 1, 2 and 3 months after modeling, and the trend of the change was also observed. Results One month after modeling, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood

  10. Renal denervation in heart failure with normal left ventricular ejection fraction. Rationale and design of the DIASTOLE (DenervatIon of the renAl Sympathetic nerves in hearT failure with nOrmal Lv Ejection fraction) trial.

    Science.gov (United States)

    Verloop, Willemien L; Beeftink, Martine M A; Nap, Alex; Bots, Michiel L; Velthuis, Birgitta K; Appelman, Yolande E; Cramer, Maarten-Jan; Agema, Willem R P; Scholtens, Asbjorn M; Doevendans, Pieter A; Allaart, Cor P; Voskuil, Michiel

    2013-12-01

    Aim Increasing evidence suggests an important role for hyperactivation of the sympathetic nervous system (SNS) in the clinical phenomena of heart failure with normal LVEF (HFNEF) and hypertension. Moreover, the level of renal sympathetic activation is directly related to the severity of heart failure. Since percutaneous renal denervation (pRDN) has been shown to be effective in modulating elevated SNS activity in patients with hypertension, it can be hypothesized that pRDN has a positive effect on HFNEF. The DIASTOLE trial will investigate whether renal sympathetic denervation influences parameters of HFNEF. Methods DIASTOLE is a multicentre, randomized controlled trial. Sixty patients, diagnosed with HFNEF and treated for hypertension, will be randomly allocated in a 1:1 ratio to undergo renal denervation on top of medical treatment (n = 30) or to maintain medical treatment alone (n = 30). The primary objective is to investigate the efficacy of pRDN by means of pulsed wave Doppler echocardiographic parameters. Secondary objectives include safety of pRDN and a comparison of changes in the following parameters after pRDN: LV mass, LV volume, LVEF, and left atrial volume as determined by magnetic resonance imaging. Also, MIBG (metaiodobenzylguanidine) uptake and washout, BNP levels, blood pressure, heart rate variability, exercise capacity, and quality of life will be assessed. Perspective DIASTOLE is a randomized controlled trial evaluating renal denervation as a treatment option for HFNEF. The results of the current trial will provide important information regarding the treatment of HFNEF, and therefore may have major impact on future therapeutic strategies. Trail registration NCT01583881.

  11. Renal nerves and nNOS

    DEFF Research Database (Denmark)

    Kompanowska-Jezierska, Elzbieta; Wolff, Helle; Kuczeriszka, Marta

    2008-01-01

    It was hypothesized that renal sympathetic nerve activity (RSNA) and neuronal nitric oxide synthase (nNOS) are involved in the acute inhibition of renin secretion and the natriuresis following slow NaCl loading (NaLoad) and that RSNA participates in the regulation of arterial blood pressure (MABP......). This was tested by NaLoad after chronic renal denervation with and without inhibition of nNOS by S-methyl-thiocitrulline (SMTC). In addition, the acute effects of renal denervation on MABP and sodium balance were assessed. Rats were investigated in the conscious, catheterized state, in metabolic cages...... of acutely and chronically denervated rats were less than control (15% and 9%, respectively, P renal denervation (14.5 +/- 0.2 vs. 19.3 +/- 1.3 mIU/l, P

  12. Resting Afferent Renal Nerve Discharge and Renal Inflammation: Elucidating the Role of Afferent and Efferent Renal Nerves in Deoxycorticosterone Acetate Salt Hypertension.

    Science.gov (United States)

    Banek, Christopher T; Knuepfer, Mark M; Foss, Jason D; Fiege, Jessica K; Asirvatham-Jeyaraj, Ninitha; Van Helden, Dusty; Shimizu, Yoji; Osborn, John W

    2016-12-01

    Renal sympathetic denervation (RDNx) has emerged as a novel therapy for hypertension; however, the therapeutic mechanisms remain unclear. Efferent renal sympathetic nerve activity has recently been implicated in trafficking renal inflammatory immune cells and inflammatory chemokine and cytokine release. Several of these inflammatory mediators are known to activate or sensitize afferent nerves. This study aimed to elucidate the roles of efferent and afferent renal nerves in renal inflammation and hypertension in the deoxycorticosterone acetate (DOCA) salt rat model. Uninephrectomized male Sprague-Dawley rats (275-300 g) underwent afferent-selective RDNx (n=10), total RDNx (n=10), or Sham (n=10) and were instrumented for the measurement of mean arterial pressure and heart rate by radiotelemetry. Rats received 100-mg DOCA (SC) and 0.9% saline for 21 days. Resting afferent renal nerve activity in DOCA and vehicle animals was measured after the treatment protocol. Renal tissue inflammation was assessed by renal cytokine content and T-cell infiltration and activation. Resting afferent renal nerve activity, expressed as a percent of peak afferent nerve activity, was substantially increased in DOCA than in vehicle (35.8±4.4 versus 15.3±2.8 %Amax). The DOCA-Sham hypertension (132±12 mm Hg) was attenuated by ≈50% in both total RDNx (111±8 mm Hg) and afferent-selective RDNx (117±5 mm Hg) groups. Renal inflammation induced by DOCA salt was attenuated by total RDNx and unaffected by afferent-selective RDNx. These data suggest that afferent renal nerve activity may mediate the hypertensive response to DOCA salt, but inflammation may be mediated primarily by efferent renal sympathetic nerve activity. Also, resting afferent renal nerve activity is elevated in DOCA salt rats, which may highlight a crucial neural mechanism in the development and maintenance of hypertension. © 2016 American Heart Association, Inc.

  13. Angiotensin II, sympathetic nerve activity and chronic heart failure.

    Science.gov (United States)

    Wang, Yutang; Seto, Sai-Wang; Golledge, Jonathan

    2014-03-01

    Sympathetic nerve activity has been reported to be increased in both humans and animals with chronic heart failure. One of the mechanisms believed to be responsible for this phenomenon is increased systemic and cerebral angiotensin II signaling. Plasma angiotensin II is increased in humans and animals with chronic heart failure. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites during chronic heart failure. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus, the rostral ventrolateral medulla and the area postrema. Blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the paraventricular nucleus. Injection of an angiotensin receptor blocker into the area postrema activates the sympathoinhibitory baroreflex. In peripheral regions, angiotensin II elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings, which may contribute to the increase in sympathetic nerve activity seen in chronic heart failure. Increased circulating angiotensin II during chronic heart failure may enhance the sympathoexcitatory chemoreflex and inhibit the sympathoinhibitory baroreflex. In addition, increased circulating angiotensin II can directly act on the central nervous system via the subfornical organ and the area postrema to increase sympathetic outflow. Inhibition of angiotensin II formation and its type 1 receptor has been shown to have beneficial effects in chronic heart failure patients.

  14. The morphological substrate for Renal Denervation : Nerve distribution patterns and parasympathetic nerves. A post-mortem histological study

    NARCIS (Netherlands)

    van Amsterdam, Wouter A C; Blankestijn, Peter J; Goldschmeding, Roel; Bleys, Ronald L A W

    2015-01-01

    BACKGROUND: Renal Denervation as a possible treatment for hypertension has been studied extensively, but knowledge on the distribution of nerves surrounding the renal artery is still incomplete. While sympathetic and sensory nerves have been demonstrated, there is no mention of the presence of paras

  15. The morphological substrate for Renal Denervation : Nerve distribution patterns and parasympathetic nerves. A post-mortem histological study

    NARCIS (Netherlands)

    van Amsterdam, Wouter A C; Blankestijn, Peter J; Goldschmeding, Roel; Bleys, Ronald L A W

    2015-01-01

    BACKGROUND: Renal Denervation as a possible treatment for hypertension has been studied extensively, but knowledge on the distribution of nerves surrounding the renal artery is still incomplete. While sympathetic and sensory nerves have been demonstrated, there is no mention of the presence of

  16. Sympathetic nerves bridge the cross-transmission in hemifacial spasm.

    Science.gov (United States)

    Zheng, Xuesheng; Hong, Wenyao; Tang, Yinda; Wu, Zhenghai; Shang, Ming; Zhang, Wenchuan; Zhong, Jun; Li, Shiting

    2012-05-23

    The pathophysiologic basis of hemifacial spasm is abnormal cross-transmission between facial nerve fibers. The author hypothesized that the demyelinated facial nerve fibers were connected with the sympathetic nerve fibers on the offending artery wall, and thus the latter function as a bridge in the cross-transmission circuit. This hypothesis was tested using a rat model of hemifacial spasm. A facial muscle response was recorded while the offending artery wall was electrically stimulated. The nerve fibers on the offending artery wall were blocked with lidocaine, or the superior cervical ganglion, which innervates the offending artery, was resected, and meanwhile the abnormal muscle response was monitored and analyzed. A waveform was recorded from the facial muscle when the offending artery wall was stimulated, named as "Z-L response". The latency of Z-L response was different from that of abnormal muscle response. When the nerve fibers on the offending artery wall were blocked by lidocaine, the abnormal muscle response disappeared gradually and recovered in 2h. The abnormal muscle response disappeared permanently after the sympathetic ganglion was resected. Our findings indicate that cross-transmission between the facial nerve fibers is bridged by the nerve fibers on the offending artery wall, probably sympathetic nerve fibers.

  17. 肾交感神经射频消融术治疗高血压犬的适宜消融温度探讨%Suitable ablation temperature for renal sympathetic-nerve ablation in treatment of hypertensive dogs

    Institute of Scientific and Technical Information of China (English)

    李慧杰; 杨成明; 余航; 曾春雨; 方玉强; 何多芬; 张小群; 温春兰

    2012-01-01

    Objective To investigate the suitable ablation temperature for renal sympathetic-nerve ablation for hypertension. Methods The canine model of hypertension was established by abdominal aortic constriction. Twenty healthy hybrid dogs, weighing 15 to 20 kg, were randomly divided into treatment group which underwent renal sympathetic-nerve ablation and control group (n = 10). Ten dogs in treatment group were randomly divided into 45 ℃ and 50 ℃ groups (n = 5) according to predetermined ablation temperature. Ablation was carried out in 1 month after modeling. Systolic blood pressure (SBP) , diastolic blood pressure (DBP) and mean arterial pressure (MAP) were measured before modeling as well as before ablation, 1 and 2 months after ablation, respectively. Renal angiography was carried out in treatment group in 2 months after ablation. Renal artery vessels were examined pathologically with HE staining. Results At 1 month after modeling, blood pressure (BP) was increased significantly in both groups (P <0.01). At 1 month after ablation, SBP was reduced significantly in treatment group (P <0.05). At 2 months after ablation, SBP, DBP and MAP were markedly lower than those before ablation ( P < 0.05, 0.01) as well as those in control group (P < 0.05, 0.01). No artery stenosis or other abnormality was observed in renal angiography review. Pathological results revealed that renal vascular injury was much more severe in 50 ℃ group than in 45 ℃ group. Conclusion 45 ℃ can be used as a conventional ablation temperature for renal sympathetic-nerve ablation for hypertension.%目的 探讨肾交感神经射频消融术治疗高血压的适宜消融温度.方法 成年健康杂种犬20只,雌雄不拘,体质量15~25 kg,建立腹主动脉缩窄型高血压模型后,随机分为治疗组(行双侧肾交感神经射频消融术)和对照组(n=10).治疗组根据预置消融温度随机分为45℃和50℃组(n=5).20只犬分别于建模前、建模后1(射频消融术前)、2(

  18. Role of sympathetic nerve activity in the process of fainting

    Directory of Open Access Journals (Sweden)

    Satoshi eIwase

    2014-09-01

    Full Text Available Syncope is defined as a transient loss of consciousness and postural tone, characterized by rapid onset, short duration, and spontaneous recovery, and the process of syncope progression will be described with two types of sympathetic change. Simultaneous recordings of microneurographically recorded MSNA and continuous and noninvasive blood pressure measurement have disclose what is going on in the course of progression of the syncope. Vasovagal or neurally mediated syncope, three stages are identified in the course of syncope onset, oscillation, imbalance, and catastrophe phases. The vasovagal syncope is characterized by the sympathoexcitation, followed by vagal overcome via the Bezold-Jarisch reflex. Orthostatic syncope is caused by the response failure or lack of sympathetic nerve activity toward the orthostatic challenge followed by the fluid shift, and subsequent cerebral low perfusion. Four causes are considered for the compensatory failure, which triggers the orthostatic syncope; hypovolemia, increased pooling in the lower body, failure to activate the sympathetic activity, and failure of vasoconstriction against sympathetic vasoconstrictive stimulation. Many pathophysiological conditions were described in the viewpoint of 1 exaggerated sympathoexcitation and 2 failure to activate the sympathetic nerve. We conclude that the sympathetic nervous system can control the cardiovascular function, and its failure resulted syncope, however, responses of the system by microneurographically recorded MSNA would determine the pathophysiology of the onset and progression of syncope, explaining the treatment effect that could be achieved by the analysis of this mechanism.

  19. Sympathetic Nerves in Breast Cancer: Angiogenesis and Antiangiogenic Therapy

    Science.gov (United States)

    2013-02-01

    decreased TH synthesis or an accelerated rate of NE uptake into sympathetic nerve terminals (6). To confirm that NE in the synapse is increased with DMI...21. Dimitrijevic M, Pilipovic I, Stanojevic S, Mitic K, Radojevic K, Pesic V, et al. Chronic propranolol treatment affects expression of

  20. A brain leptin-renin angiotensin system interaction in the regulation of sympathetic nerve activity

    Science.gov (United States)

    Hilzendeger, Aline M.; Morgan, Donald A.; Brooks, Leonard; Dellsperger, David; Liu, Xuebo; Grobe, Justin L.; Rahmouni, Kamal; Sigmund, Curt D.

    2012-01-01

    The sympathetic nervous system, leptin, and renin-angiotensin system (RAS) have been implicated in obesity-associated hypertension. There is increasing evidence for the presence of both leptin and angiotensin II receptors in several key brain cardiovascular and metabolic control regions. We tested the hypothesis that the brain RAS plays a facilitatory role in the sympathetic nerve responses to leptin. In rats, intracerebroventricular (ICV) administration of losartan (5 μg) selectively inhibited increases in renal and brown adipose tissue (BAT) sympathetic nerve activity (SNA) produced by leptin (10 μg ICV) but did not reduce the SNA responses to corticotrophin-releasing factor (CRF) or the melanocortin receptor agonist MTII. In mice with deletion of angiotensin II type-1a receptors (AT1aR−/−), increases in renal and BAT SNA induced by leptin (2 μg ICV) were impaired whereas SNA responses to MTII were preserved. Decreases in food intake and body weight with ICV leptin did not differ in AT1aR−/− vs. AT1aR+/+ mice. ICV leptin in rats increased AT1aR and angiotensin-converting enzyme (ACE) mRNA in the subfornical organ and AT1aR mRNA in the arcuate nucleus, suggesting leptin-induced upregulation of the brain RAS in specific brain regions. To evaluate the role of de novo production of brain angiotensin II in SNA responses to leptin, we treated rats with captopril (12.5 μg ICV). Captopril attenuated leptin effects on renal and BAT SNA. In conclusion, these studies provide evidence that the brain RAS selectively facilitates renal and BAT sympathetic nerve responses to leptin while sparing effects on food intake. PMID:22610169

  1. Cardiac fibroblasts regulate sympathetic nerve sprouting and neurocardiac synapse stability.

    Directory of Open Access Journals (Sweden)

    Céline Mias

    Full Text Available Sympathetic nervous system (SNS plays a key role in cardiac homeostasis and its deregulations always associate with bad clinical outcomes. To date, little is known about molecular mechanisms regulating cardiac sympathetic innervation. The aim of the study was to determine the role of fibroblasts in heart sympathetic innervation. RT-qPCR and western-blots analysis performed in cardiomyocytes and fibroblasts isolated from healthy adult rat hearts revealed that Pro-Nerve growth factor (NGF and pro-differentiating mature NGF were the most abundant neurotrophins expressed in cardiac fibroblasts while barely detectable in cardiomyocytes. When cultured with cardiac fibroblasts or fibroblast-conditioned medium, PC12 cells differentiated into/sympathetic-like neurons expressing axonal marker Tau-1 at neurites in contact with cardiomyocytes. This was prevented by anti-NGF blocking antibodies suggesting a paracrine action of NGF secreted by fibroblasts. When co-cultured with cardiomyocytes to mimic neurocardiac synapse, differentiated PC12 cells exhibited enhanced norepinephrine secretion as quantified by HPLC compared to PC12 cultured alone while co-culture with fibroblasts had no effect. However, when supplemented to PC12-cardiomyocytes co-culture, fibroblasts allowed long-term survival of the neurocardiac synapse. Activated fibroblasts (myofibroblasts isolated from myocardial infarction rat hearts exhibited significantly higher mature NGF expression than normal fibroblasts and also promoted PC12 cells differentiation. Within the ischemic area lacking cardiomyocytes and neurocardiac synapses, tyrosine hydroxylase immunoreactivity was increased and associated with local anarchical and immature sympathetic hyperinnervation but tissue norepinephrine content was similar to that of normal cardiac tissue, suggesting depressed sympathetic function. Collectively, these findings demonstrate for the first time that fibroblasts are essential for the setting of

  2. Cardiac Fibroblasts Regulate Sympathetic Nerve Sprouting and Neurocardiac Synapse Stability

    Science.gov (United States)

    Mias, Céline; Coatrieux, Christelle; Denis, Colette; Genet, Gaël; Seguelas, Marie-Hélène; Laplace, Nathalie; Rouzaud-Laborde, Charlotte; Calise, Denis; Parini, Angelo; Cussac, Daniel; Pathak, Atul; Sénard, Jean-Michel; Galés, Céline

    2013-01-01

    Sympathetic nervous system (SNS) plays a key role in cardiac homeostasis and its deregulations always associate with bad clinical outcomes. To date, little is known about molecular mechanisms regulating cardiac sympathetic innervation. The aim of the study was to determine the role of fibroblasts in heart sympathetic innervation. RT-qPCR and western-blots analysis performed in cardiomyocytes and fibroblasts isolated from healthy adult rat hearts revealed that Pro-Nerve growth factor (NGF) and pro-differentiating mature NGF were the most abundant neurotrophins expressed in cardiac fibroblasts while barely detectable in cardiomyocytes. When cultured with cardiac fibroblasts or fibroblast-conditioned medium, PC12 cells differentiated into/sympathetic-like neurons expressing axonal marker Tau-1 at neurites in contact with cardiomyocytes. This was prevented by anti-NGF blocking antibodies suggesting a paracrine action of NGF secreted by fibroblasts. When co-cultured with cardiomyocytes to mimic neurocardiac synapse, differentiated PC12 cells exhibited enhanced norepinephrine secretion as quantified by HPLC compared to PC12 cultured alone while co-culture with fibroblasts had no effect. However, when supplemented to PC12-cardiomyocytes co-culture, fibroblasts allowed long-term survival of the neurocardiac synapse. Activated fibroblasts (myofibroblasts) isolated from myocardial infarction rat hearts exhibited significantly higher mature NGF expression than normal fibroblasts and also promoted PC12 cells differentiation. Within the ischemic area lacking cardiomyocytes and neurocardiac synapses, tyrosine hydroxylase immunoreactivity was increased and associated with local anarchical and immature sympathetic hyperinnervation but tissue norepinephrine content was similar to that of normal cardiac tissue, suggesting depressed sympathetic function. Collectively, these findings demonstrate for the first time that fibroblasts are essential for the setting of cardiac sympathetic

  3. The role of the renal afferent and efferent nerve fibers in heart failure.

    Science.gov (United States)

    Booth, Lindsea C; May, Clive N; Yao, Song T

    2015-01-01

    Renal nerves contain afferent, sensory and efferent, sympathetic nerve fibers. In heart failure (HF) there is an increase in renal sympathetic nerve activity (RSNA), which can lead to renal vasoconstriction, increased renin release and sodium retention. These changes are thought to contribute to renal dysfunction, which is predictive of poor outcome in patients with HF. In contrast, the role of the renal afferent nerves remains largely unexplored in HF. This is somewhat surprising as there are multiple triggers in HF that have the potential to increase afferent nerve activity, including increased venous pressure and reduced kidney perfusion. Some of the few studies investigating renal afferents in HF have suggested that at least the sympatho-inhibitory reno-renal reflex is blunted. In experimentally induced HF, renal denervation, both surgical and catheter-based, has been associated with some improvements in renal and cardiac function. It remains unknown whether the effects are due to removal of the efferent renal nerve fibers or afferent renal nerve fibers, or a combination of both. Here, we review the effects of HF on renal efferent and afferent nerve function and critically assess the latest evidence supporting renal denervation as a potential treatment in HF.

  4. The Potential Role of Catheter-Based Renal Sympathetic Denervation in Chronic and End-Stage Kidney Disease.

    Science.gov (United States)

    Sata, Yusuke; Schlaich, Markus P

    2016-07-01

    Sympathetic activation is a hallmark of chronic and end-stage renal disease and adversely affects cardiovascular prognosis. Hypertension is present in the vast majority of these patients and plays a key role in the progressive deterioration of renal function and the high rate of cardiovascular events in this patient cohort. Augmentation of renin release, tubular sodium reabsorption, and renal vascular resistance are direct consequences of efferent renal sympathetic nerve stimulation and the major components of neural regulation of renal function. Renal afferent nerve activity directly influences sympathetic outflow to the kidneys and other highly innervated organs involved in blood pressure control via hypothalamic integration. Renal denervation of the kidney has been shown to reduce blood pressure in many experimental models of hypertension. Targeting the renal nerves directly may therefore be specifically useful in patients with chronic and end-stage renal disease. In this review, we will discuss the potential role of catheter-based renal denervation in patients with impaired kidney function and also reflect on the potential impact on other cardiovascular conditions commonly associated with chronic kidney disease such as heart failure and arrhythmias.

  5. Causes and consequences of increased sympathetic activity in renal disease

    NARCIS (Netherlands)

    Joles, JA; Koomans, HA

    2004-01-01

    Much evidence indicates increased sympathetic nervous activity (SNA) in renal disease. Renal ischemia is probably a primary event leading to increased SNA. Increased SNA often occurs in association with hypertension. However, the deleterious effect of increased SNA on the diseased kidney is not only

  6. Cardiac sympathetic nerve terminal function in congestive heart failure

    Institute of Scientific and Technical Information of China (English)

    Chang-seng LIANG

    2007-01-01

    Increased cardiac release of norepinephrine (NE) and depleted cardiac stores of NE are two salient features of the human failing heart. Researches from my labo-ratory have shown that these changes are accompanied by a functional defect of NE uptake in the cardiac sympathetic nerve terminals. Our studies have shown that the decrease of NE uptake is caused by reduction of NE transporter density in the sympathetic nerve endings, and this change is responsible, at least in part, for the increased myocardial interstitial NE, decreased myocardial adrenoceptor density, and increased myocyte apoptosis in experimental cardiomyopathies. We have also provided evidence in both intact animals and cultured PC12 cells that the decrease of NE transporter is induced by the actions of oxidative metabolites of exogenous NE, involving endoplasmic reticulum stress and impaired N-glycosylation of the NE transporter. This change in the cardiac sympathetic NE uptake function, as demonstrated by [123I] metaiodobenzylguanidine in human studies, may not only serve as an important prognostic variable in patients with congestive heart failure, but also be used as a surrogate for the efficacies of various therapeutic interventions for heart failure. Finally, increasing evidence suggests and further studies are needed to show that the cardiac sympathetic nerve terminal function may be a direct target for pharmacologic treatment of congestive heart failure.

  7. Nerve Growth Factor Decreases in Sympathetic and Sensory Nerves of Rats with Chronic Heart Failure

    Science.gov (United States)

    Lu, Jian

    2014-01-01

    Nerve growth factor (NGF) plays a critical role in the maintenance and survival of both sympathetic and sensory nerves. Also, NGF can regulate receptor expression and neuronal activity in the sympathetic and sensory neurons. Abnormalities in NGF regulation are observed in patients and animals with heart failure (HF). Nevertheless, the effects of chronic HF on the levels of NGF within the sympathetic and sensory nerves are not known. Thus, the ELISA method was used to assess the levels of NGF in the stellate ganglion (SG) and dorsal root ganglion (DRG) neurons of control rats and rats with chronic HF induced by myocardial infarction. Our data show for the first time that the levels of NGF were significantly decreased (P < 0.05) in the SG and DRG neurons 6–20 weeks after ligation of the coronary artery. In addition, a close relation was observed between the NGF levels and the left ventricular function. In conclusion, chronic HF impairs the expression of NGF in the sympathetic and sensory nerves. Given that sensory afferent nerves are engaged in the sympathetic nervous responses to somatic stimulation (i.e. muscle activity during exercise) via a reflex mechanism, our data indicate that NGF is likely responsible for the development of muscle reflex-mediated abnormal sympathetic responsiveness observed in chronic HF. PMID:24913185

  8. Do sympathetic nerves release noradrenaline in "quanta"?

    Science.gov (United States)

    Stjärne, L

    2000-07-01

    The discovery of excitatory junction potentials (EJPs) in guinea-pig vas deferens by Burnstock and Holman (1960) showed for the first time that a sympathetic transmitter, now known to be ATP, is secreted in "quanta". As it was assumed at the time that EJPS are triggered by noradrenaline, this discovery led to attempts to use the fractional overflow of noradrenaline from sympathetically innervated tissues to assess, indirectly, the number of noradrenaline molecules in the average "quantum". The basic finding was that each pulse released 1/50000 of the tissue content of noradrenaline, when reuptake was blocked and prejunctional alpha(2)-adrenoceptors were intact. This provided the constraints, two extreme alternatives: (i) each pulse releases 0.2-3% of the content of a vesicle from all varicosities, or (ii) each pulse releases the whole content of a vesicle from 0.2 to 3% of the varicosities. New techniques have made it possible to address questions about the release probability in individual sites, or the "quantal" size, more directly. Results by optical (comparison of the labelling of SV2 and synaptotagmin, proteins in the membrane of transmitter vesicles), electrophysiological (excitatory junction currents, EJCs, at single visualized varicosities) and amperometric (the noradrenaline oxidation current at a carbon fibre electrode) methods reveal that transmitter exocytosis in varicosities is intermittent. The EJC and noradrenaline oxidation current responses (in rat arteries) to a train of single pulses were observed to be similar in intermittency and amplitude fluctuation. This suggests that they are caused by exocytosis of single or very few "quanta" of ATP and noradrenaline, respectively, equal to the contents of single vesicles, from a small population of release sites. These findings support, but do not conclusively prove the validity of the "intermittent" model of noradrenaline release. The question if noradrenaline is always secreted in packets of preset size

  9. Device-based approaches for renal nerve ablation for hypertension and beyond

    Directory of Open Access Journals (Sweden)

    Alicia Ann Thorp

    2015-07-01

    Full Text Available Animal and human studies have demonstrated that chronic activation of renal sympathetic nerves is critical in the pathogenesis and perpetuation of treatment-resistant hypertension. Bilateral renal denervation has emerged as a safe and effective, non-pharmacological treatment for resistant hypertension that involves the selective ablation of efferent and afferent renal nerves to lower blood pressure. However, the most recent and largest randomized controlled trial failed to confirm the primacy of renal denervation over a sham procedure, prompting widespread re-evaluation of the therapy’s efficacy. Disrupting renal afferent sympathetic signalling to the hypothalamus with renal denervation lowers central sympathetic tone, which has the potential to confer additional clinical benefits beyond blood pressure control. Specifically, there has been substantial interest in the use of renal denervation as either a primary or adjunct therapy in pathological conditions characterized by central sympathetic over-activity such as renal disease, heart failure and metabolic-associated disorders. Recent findings from pre-clinical and proof-of–concept studies appear promising with renal denervation shown to confer cardiovascular and metabolic benefits, largely independent of changes in blood pressure. This review explores the pathological rationale for targeting sympathetic renal nerves for blood pressure control. Latest developments in renal nerve ablation modalities designed to improve procedural success are discussed along with prospective findings on the efficacy of renal denervation to lower blood pressure in treatment-resistant hypertensive patients. Preliminary evidence in support of renal denervation as a possible therapeutic option in disease states characterized by central sympathetic over-activity is also presented.

  10. MR-guided Periarterial Ethanol Injection for Renal Sympathetic Denervation: A Feasibility Study in Pigs

    Energy Technology Data Exchange (ETDEWEB)

    Streitparth, F., E-mail: florian.streitparth@charite.de; Walter, A.; Stolzenburg, N.; Heckmann, L.; Breinl, J. [Charite, Humboldt University, Department of Radiology (Germany); Rinnenthal, J. L. [Charite, Humboldt University, Department of Neuropathology (Germany); Beck, A.; De Bucourt, M.; Schnorr, J. [Charite, Humboldt University, Department of Radiology (Germany); Bernhardt, U. [InnoRa GmbH (Germany); Gebauer, B.; Hamm, B.; Guenther, R. W. [Charite, Humboldt University, Department of Radiology (Germany)

    2013-06-15

    Purpose. To evaluate the feasibility and efficacy of image-guided periarterial ethanol injection as an alternative to transluminal radiofrequency ablation. Methods. Unilateral renal periarterial ethanol injection was performed under general anesthesia in 6 pigs with the contralateral kidney serving as control. All interventions were performed in an open 1.0 T MRI system under real-time multiplanar guidance. The injected volume was 5 ml (95 % ethanol labelled marked MR contrast medium) in 2 pigs and 10 ml in 4 pigs. Four weeks after treatment, the pigs underwent MRI including MRA and were killed. Norepinephrine (NE) concentration in the renal parenchyma served as a surrogate parameter to analyze the efficacy of sympathetic denervation. In addition, the renal artery and sympathetic nerves were examined histologically to identify evidence of vascular and neural injury. Results. In pigs treated with 10 ml ethanol, treatment resulted in neural degeneration. We found a significant reduction of NE concentration in the kidney parenchyma of 53 % (p < 0.02) compared with the untreated contralateral kidney. In pigs treated with 5 ml ethanol, no significant changes in histology or NE were observed. There was no evidence of renal arterial stenosis in MRI, macroscopy or histology in any pig. Conclusion. MR-guided periarterial ethanol injection was feasible and efficient for renal sympathetic denervation in a swine model. This technique may be a promising alternative to the catheter-based approach in the treatment of resistant arterial hypertension.

  11. Moxonidine normalizes sympathetic hyperactivity in patients with eprosartan-treated chronic renal failure.

    Science.gov (United States)

    Neumann, Jutta; Ligtenberg, Gerry; Oey, Liam; Koomans, Hein A; Blankestijn, Peter J

    2004-11-01

    Enalapril and losartan reduce but not normalize sympathetic hyperactivity in patients with hypertensive chronic renal failure (CRF). This study assessed the effect of chronic eprosartan on BP and sympathetic activity, and assessed the effect of moxonidine during chronic eprosartan treatment. In 11 stable patients with CRF (creatinine clearance 47 +/- 10 ml/min), muscle sympathetic nerve activity (MSNA; peroneal nerve), BP, and baroreceptor sensitivity were measured in the absence of antihypertensive drugs (except diuretics) during chronic eprosartan therapy (600 mg for 6 wk) and in 9 patients after moxonidine (0.2 mg for 6 wk) was added. Normovolemia was controlled by diuretics and confirmed by extracellular fluid volume measurements. BP, heart rate, and MSNA were higher in patients than in 22 controls. During eprosartan therapy, mean arterial pressure (111 +/- 9 to 98 +/- 7 mmHg, P < 0.001), heart rate (71 +/- 10 to 65 +/- 8 bpm, P < 0.001), and MSNA (35 +/- 10 to 27 +/- 8 bursts/min, P < 0.001) decreased. After the addition of moxonidine (n = 9), a further reduction of mean arterial pressure to 89 +/- 7 mmHg (P < 0.05) and of MSNA to 20 +/- 10 bursts/min (P < 0.05) occurred. Sympathetic activity in patients with CRF can be normalized, and angiotensin II-independent sympathetic hyperactivity contributes to the pathogenesis of renal hypertension. Sympathetic hyperactivity is associated with poor cardiovascular outcomes, implying that reduction might be beneficial to the patients. The addition of moxonidine to angiotensin II antagonist treatment might be appropriate.

  12. Sympathetic nerve activity and simulated diving in healthy humans.

    Science.gov (United States)

    Shamsuzzaman, Abu; Ackerman, Michael J; Kuniyoshi, Fatima Sert; Accurso, Valentina; Davison, Diane; Amin, Raouf S; Somers, Virend K

    2014-04-01

    The goal of our study was to develop a simple and practical method for simulating diving in humans using facial cold exposure and apnea stimuli to measure neural and circulatory responses during the stimulated diving reflex. We hypothesized that responses to simultaneous facial cold exposure and apnea (simulated diving) would be synergistic, exceeding the sum of responses to individual stimuli. We studied 56 volunteers (24 female and 32 male), average age of 39 years. All subjects were healthy, free of cardiovascular and other diseases, and on no medications. Although muscle sympathetic nerve activity (MSNA), blood pressure, and vascular resistance increased markedly during both early and late phases of simulated diving, significant reductions in heart rate were observed only during the late phase. Total MSNA during simulated diving was greater than combined MSNA responses to the individual stimuli. We found that simulated diving is a powerful stimulus to sympathetic nerve traffic with significant bradycardia evident in the late phase of diving and eliciting synergistic sympathetic and parasympathetic responses. Our data provide insight into autonomic triggers that could help explain catastrophic cardiovascular events that may occur during asphyxia or swimming, such as in patients with obstructive sleep apnea or congenital long QT syndrome.

  13. Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

    Science.gov (United States)

    Ramchandra, Rohit; Hood, Sally G.; Denton, Derek A.; Woods, Robin L.; McKinley, Michael J.; McAllen, Robin M.; May, Clive N.

    2009-01-01

    In heart failure (HF), sympathetic nerve activity is increased. Measurements in HF patients of cardiac norepinephrine spillover, reflecting cardiac sympathetic nerve activity (CSNA), indicate that it is increased earlier and to a greater extent than sympathetic activity to other organs. This has important consequences because it worsens prognosis, provoking arrhythmias and sudden death. To elucidate the mechanisms responsible for the activation of CSNA in HF, we made simultaneous direct neural recordings of CSNA and renal SNA (RSNA) in two groups of conscious sheep: normal animals and animals in HF induced by chronic, rapid ventricular pacing. In normal animals, the level of activity, measured as burst incidence (bursts of pulse related activity/100 heart beats), was significantly lower for CSNA (30 ± 5%) than for RSNA (94 ± 2%). Furthermore, the resting level of CSNA, relative to its maximum achieved while baroreceptors were unloaded by reducing arterial pressure, was set at a much lower percentage than RSNA. In HF, burst incidence of CSNA increased from 30 to 91%, whereas burst incidence of RSNA remained unaltered at 95%. The sensitivity of the control of both CSNA and RSNA by the arterial baroreflex remained unchanged in HF. These data show that, in the normal state, the resting level of CSNA is set at a lower level than RSNA, but in HF, the resting levels of SNA to both organs are close to their maxima. This finding provides an explanation for the preferential increase in cardiac norepinephrine spillover observed in HF. PMID:19136635

  14. Effect of sympathetic nerve block on acute inflammatory pain and hyperalgesia

    DEFF Research Database (Denmark)

    Pedersen, J L; Rung, G W; Kehlet, H

    1997-01-01

    BACKGROUND: Sympathetic nerve blocks relieve pain in certain chronic pain states, but the role of the sympathetic pathways in acute pain is unclear. Thus the authors wanted to determine whether a sympathetic block could reduce acute pain and hyperalgesia after a heat injury in healthy volunteers....

  15. Insulin acts in the arcuate nucleus to increase lumbar sympathetic nerve activity and baroreflex function in rats

    National Research Council Canada - National Science Library

    Cassaglia, Priscila A; Hermes, Sam M; Aicher, Sue A; Brooks, Virginia L

    2011-01-01

    Non‐technical summary  Though the pancreatic hormone insulin is known to act in the brain to increase sympathetic nerve activity and baroreflex control of sympathetic nerve activity, its specific site of action had yet to be identified...

  16. Leptin signaling in the nucleus tractus solitarii increases sympathetic nerve activity to the kidney.

    Science.gov (United States)

    Mark, Allyn L; Agassandian, Khristofor; Morgan, Donald A; Liu, Xuebo; Cassell, Martin D; Rahmouni, Kamal

    2009-02-01

    The hypothalamic arcuate nucleus was initially regarded as the principal site of leptin action, but there is increasing evidence for functional leptin receptors in extrahypothalamic sites, including the nucleus tractus solitarii (NTS). We demonstrated previously that arcuate injection of leptin increases sympathetic nerve activity (SNA) to brown adipose tissue and kidney. In this study, we tested the hypothesis that leptin signaling in the NTS affects sympathetic neural outflow. Using a stereotaxic device in anesthetized rats, we microinjected leptin (0.25 to 1.00 microg) or saline into the NTS while recording SNA to kidney and brown adipose tissue. Microinjection of leptin into the commissural and medial subnuclei of the caudal NTS at the level of the area postrema in Sprague-Dawley rats produced a dose-related increase in renal SNA (+112+/-15% with leptin 1 microg; n=7; Pleptin receptors, because it was not observed in Zucker obese rats that have a missense mutation in the leptin receptor. Rostral NTS injection of leptin failed to increase SNA, indicating that leptin signaling in the NTS is probably confined to the caudal NTS at the level of the area postrema. In summary, this study demonstrates that leptin signaling in the caudal NTS increases SNA to the kidney but not to the brown adipose tissue. The study strengthens the concept of a distributed brain network of leptin action and demonstrates that these distributed brain sites can mediate contrasting sympathetic responses to leptin.

  17. Study of nerve fibers nature reinforcing duodenal contractions by electrical stimulation of sympathetic nerve

    Directory of Open Access Journals (Sweden)

    Sveshnikov D.S.

    2011-09-01

    Full Text Available The subject of the article is to investigate the mechanism of increased reactions by electrical stimulation of the sympathetic nerve. Materials and methods: Experiments on dogs have shown that stimulant reactions during blockade of a-adrenergic by phentolamine and (3-adrenergic receptors with propranolol were completely eliminated by lizer-gol —the blocker of 5-HT12-receptors. Results: Infusion of lizergol did not influence on duodenal motor activity and the function of the vagus nerve. Conclusion: Effector neuron is found out to be serotonergic and its action is provided by 5-HT1 2 receptors

  18. Differential effects of oestrogen on developing and mature uterine sympathetic nerves.

    Science.gov (United States)

    Chávez-Genaro, R; Crutcher, K; Viettro, L; Richeri, A; Coirolo, N; Burnstock, G; Cowen, T; Brauer, M M

    2002-04-01

    Oestrogen is a key factor in the remodelling of uterine sympathetic nerves during puberty and the oestrous cycle; these nerves are influenced by changes in their target uterine tissue. The magnitude of oestrogen-induced responses might however be influenced by the maturation stage of sympathetic nerve fibres, the age of the neurons and/or the developmental state of the uterus. We have therefore compared the sympathetic innervation of the uterus following chronic oestrogen treatment of infantile/prepubertal and young adult intact and ovariectomised rats. Treatment of infantile/prepubertal rats resulted in the complete loss of intrauterine noradrenaline (NA)-labelled sympathetic nerves and a marked reduction in the total NA content in the uterine horn. Chronic treatment of young adult rats had little effect. To examine whether the age of the neurons or the degree of development of the uterus determined responsiveness of nerves to oestrogen, we assessed the effects of oestrogen on the sympathetic reinnervation of intraocular transplants of young adult uterine myometrium into ovariectomised adult host rats. Early treatment (10 days post-transplantation) resulted in less sympathetic innervation than late treatment (30 days post-transplantation). Measurements of nerve growth factor (NGF) levels in the uterine horn of control rats before and after puberty and following infantile/prepubertal chronic oestrogen treatment and acute oestrogen treatment of young adult rats revealed a coordinated increase between the growth of the uterus and NGF protein levels. Thus, developing and recently regrown sympathetic nerves are more susceptible to oestrogen-induced changes in the uterus than mature nerves, differential susceptibility is not related to the age of the neurons or the developmental state of the uterus and changes in NGF protein do not account for the differential susceptibility of developing and mature uterine sympathetic nerve fibres to oestrogen. Growing sympathetic

  19. Aliskiren ameliorates sympathetic nerve sprouting and suppresses the inducibility of ventricular tachyarrhythmia in postinfarcted rat heart

    Institute of Scientific and Technical Information of China (English)

    JIA Yin-yu; BAO Zhi-wei; WEI Mei-fang; ZHU Jian-hua; GUI Le

    2013-01-01

    Background Aliskiren is an oral renin inhibitor,which inhibits the first rate limiting step in the renin angiotensin aldosterone system.In this study,sympathetic nerve sprouting and the inducibility of ventricular fibrillation after aliskiren treatment in myocardial infarction were investigated.Methods Male Sprague Dawley rats after coronary artery ligation were randomly allocated to four groups:angiotensin converting enzyme inhibitor enalapril,angiotensin receptor blocker valsartan,β adrenergic receptor blocker carvedilol and rennin inhibitor aliskiren treatment for six weeks.Electrophysiological study,histological examination and Western blotting were performed.Results The plasma norepinephrine level and sympathetic nerve innervation significantly increased in treated infarcted rats compared to untreated rats.Aliskiren treatment reduced the sympathetic nerve innervations after myocardial infarction.There is no significant difference in sympathetic nerve innervations after myocardial infarction among the enalapril,valsartan,carvediloand or aliskiren treated groups.Programmed electrical stimulation study showed that inducible ventricular arrhythmia was reduced,ventricular fibrillation threshold was increased and ventricular effective refractory period was prolonged in enalapril,valsartan,carvedilol and aliskiren treated infarcted rats compared to untreated infarcted rats.Cardiomyocytic apoptosis in infarcted region was significantly decreased in enalapril,valsartan,carvedilol and aliskiren treated infarcted rats.Conclusions Aliskiren ameliorated cardiomyocytic apoptosis,attenuated the sympathetic nerve innervations and reduced the vulnerability of ventricular arrhythmias after myocardial infarction.Enalapril,valsartan and carvedilol have similar effects as aliskiren on cardiomyocytic apoptosis,sympathetic nerve innervations and vulnerability of ventricular arrhythmias after myocardial infarction.

  20. Evidence of sympathetic fibers in the male rat pelvic nerve by gross anatomy, retrograde labeling and high resolution autoradiographic study.

    Science.gov (United States)

    Giuliano, F; Facchinetti, P; Bernabé, J; Benoit, G; Calas, A; Rampin, O

    1997-12-01

    Several arguments exist in various animal species and man for the presence of a sympathetic component in the pelvic nerve, classically regarded as parasympathetic. We tested this hypothesis in the male rat. Nerve bundles issued from the sacral region of the paravertebral sympathetic chain and reaching the S1 spinal nerve were identified. Neurons in the sacral parasympathetic nucleus of the L6-S1 spinal cord and in the L2-S1 paravertebral sympathetic chain were retrogradely labeled from the pelvic nerve. Radioautography evidenced labeling of unmyelinated fibers in the pelvic nerve following in vitro incubation with 3H-noradrenaline. A population of sympathetic fibers issued from the lumbosacral sympathetic chain exists in the pelvic nerve of the male rat. This qualitative study provides a morphological basis to uncover the role of the sympathetic outflow present in the pelvic nerve.

  1. Norepinephrine-induced nerve growth factor depletion causes cardiac sympathetic denervation in severe heart failure.

    Science.gov (United States)

    Kimura, Kensuke; Kanazawa, Hideaki; Ieda, Masaki; Kawaguchi-Manabe, Haruko; Miyake, Yoshiko; Yagi, Takashi; Arai, Takahide; Sano, Motoaki; Fukuda, Keiichi

    2010-08-25

    In severe congestive heart failure (CHF), sympathetic overactivity correlates with the exacerbation of cardiac performance. To test the hypothesis that the cardiac sympathetic nerve density dramatically changes with the acceleration of circulating norepinephrine (NE) concentration, we investigated the temporal association of nerve growth factor (NGF) expression in the heart and cardiac sympathetic nerve density during the development of CHF in the continuous NE-infused rats. The animals were analyzed at 0-, 1-, 3-, 7-, 14-, and 28-day after implantation of osmotic pump at a rate of 0.05 mg/kg/hr. The cardiac performance was temporally facilitated in NE-exposed rats at 3-day in accordance with the sympathetic hyper-innervation induced by the augmentation of NGF mRNA expression in the heart. In NE-treated rats, left ventricular end-diastolic pressure was significantly increased after 7-day and marked left ventricular hypertrophy and systemic fluid retention were observed at 28-day. CHF-induced sympathetic overactivity further increased plasma NE concentration in NE-treated rats and finally reached to 16.1+/-5.6 ng/ml at 28-day (control level was 0.39+/-0.1 ng/ml, pcardiac performance. The cardiac sympathetic fiber loss was also confirmed in NE-exposed DBH (dopamine beta-hydroxylase)-Cre/Floxed-EGFP (enhanced green fluorescent protein) mice with severe CHF, in which sympathetic nerve could be traced by EGFP. Our results suggest that the cardiac sympathetic nerve density is strictly regulated by the NGF expression in the heart and long-exposure of high plasma NE concentration caused myocardial NGF reduction, following sympathetic fiber loss in severe CHF animals.

  2. Effects of acute administration of selective serotonin reuptake inhibitors on sympathetic nerve activity

    Energy Technology Data Exchange (ETDEWEB)

    Tiradentes, R.V. [Departamento de Ciências Fisiológicas, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES (Brazil); Centro Universitário do Espírito Santo, Colatina, ES (Brazil); Pires, J.G.P. [Centro Universitário do Espírito Santo, Colatina, ES (Brazil); Escola de Medicina da Empresa Brasileira de Ensino, Vitória, ES (Brazil); Silva, N.F. [Departamento de Morfologia, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES (Brazil); Ramage, A.G. [Department of Neuroscience, Physiology and Pharmacology, University College London, London (United Kingdom); Santuzzi, C.H. [Departamento de Ciências Fisiológicas, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES (Brazil); Centro Universitário do Espírito Santo, Colatina, ES (Brazil); Futuro, H.A. Neto [Escola de Medicina da Empresa Brasileira de Ensino, Vitória, ES (Brazil); Departamento de Morfologia, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES (Brazil); Escola Superior de Ciências da Saúde, Santa Casa de Misericórdia de Vitória, Vitória, ES (Brazil)

    2014-05-30

    Serotonergic mechanisms have an important function in the central control of circulation. Here, the acute effects of three selective serotonin (5-HT) reuptake inhibitors (SSRIs) on autonomic and cardiorespiratory variables were measured in rats. Although SSRIs require 2-3 weeks to achieve their full antidepressant effects, it has been shown that they cause an immediate inhibition of 5-HT reuptake. Seventy male Wistar rats were anesthetized with urethane and instrumented to record blood pressure, heart rate, renal sympathetic nerve activity (RSNA), and respiratory frequency. At lower doses, the acute cardiovascular effects of fluoxetine, paroxetine and sertraline administered intravenously were insignificant and variable. At middle and higher doses, a general pattern was observed, with significant reductions in sympathetic nerve activity. At 10 min, fluoxetine (3 and 10 mg/kg) reduced RSNA by -33±4.7 and -31±5.4%, respectively, without changes in blood pressure; 3 and 10 mg/kg paroxetine reduced RSNA by -35±5.4 and -31±5.5%, respectively, with an increase in blood pressure +26.3±2.5; 3 mg/kg sertraline reduced RSNA by -59.4±8.6%, without changes in blood pressure. Sympathoinhibition began 5 min after injection and lasted approximately 30 min. For fluoxetine and sertraline, but not paroxetine, there was a reduction in heart rate that was nearly parallel to the sympathoinhibition. The effect of these drugs on the other variables was insignificant. In conclusion, acute peripheral administration of SSRIs caused early autonomic cardiovascular effects, particularly sympathoinhibition, as measured by RSNA. Although a peripheral action cannot be ruled out, such effects are presumably mostly central.

  3. Renal Sympathetic Denervation by CT-scan-Guided Periarterial Ethanol Injection in Sheep

    Energy Technology Data Exchange (ETDEWEB)

    Firouznia, Kavous, E-mail: k-firouznia@yahoo.com; Hosseininasab, Sayed jaber, E-mail: dr.hosseininasab@gmail.com [Tehran University of Medical Sciences (TMUS), Advanced Diagnostic and Interventional Radiology Research Center (ADIR), Imam Khomeini Hospital Complex (Iran, Islamic Republic of); Amanpour, Saeid, E-mail: saeidamanpour@yahoo.com [Tehran University of Medical Science, Cancer Models Research Center, Cancer Institute of Iran (Iran, Islamic Republic of); Haj-Mirzaian, Arya, E-mail: arya.mirzaian@gmail.com [Tehran University of Medical Science, Department of Radiology and Imaging, MIC, Imam Khomeini Hospital (Iran, Islamic Republic of); Miri, Roza, E-mail: rosa.miri@yahoo.com [Tehran University of Medical Science, Department of Pathology, Imam Khomeini Hospital Complex (Iran, Islamic Republic of); Muhammadnejad, Ahad, E-mail: mohamadnejad@yahoo.com [Tehran University of Medical Science, Cancer Research Center, Cancer Institute of Iran (Iran, Islamic Republic of); Muhammadnejad, Samad, E-mail: s-muhammadnejad@sina.tums.ac.ir [Tehran University of Medical Sciences, Research Center for Molecular and Cellular Imaging (Iran, Islamic Republic of); Jalali, Amir H., E-mail: amirjalali51@yahoo.com [Tehran University of Medical Sciences (TMUS), Advanced Diagnostic and Interventional Radiology Research Center (ADIR), Imam Khomeini Hospital Complex (Iran, Islamic Republic of); Ahmadi, Farrokhlagha, E-mail: ahmadi@tums.ac.ir [Tehran University of Medical Sciences, Nephrology Research Center, Imam Khomeini Hospital Complex (Iran, Islamic Republic of); Rokni-Yazdi, Hadi, E-mail: rokniyaz@tums.ac.ir [Tehran University of Medical Sciences (TMUS), Advanced Diagnostic and Interventional Radiology Research Center (ADIR), Imam Khomeini Hospital Complex (Iran, Islamic Republic of)

    2015-08-15

    BackgroundRenal nerves are a recent target in the treatment of hypertension. Renal sympathetic denervation (RSD) is currently performed using catheter-based radiofrequency ablation (RFA) and because this method has limitations, percutaneous magnetic resonance (MR)-guided periarterial ethanol injection is a suggested alternative. However, few studies have been conducted on the effectiveness of percutaneous ethanol injection for RSD.AimTo evaluate the feasibility, efficacy, and complications of computed tomography (CT)-guided periarterial ethanol injection.MethodsEthanol (10 ml, 99.6 %) was injected around the right renal artery in six sheep under CT guidance with the left kidney serving as a control. Before and after the intervention, the sheep underwent MR imaging studies and the serum creatinine level was measured. One month after the intervention, the sheep were euthanized and norepinephrine (NE) concentration in the renal parenchyma was measured to evaluate the efficacy of the procedure. The treated tissues were also examined histopathologically to evaluate vascular, parenchymal, and neural injury.ResultsThe right kidney parenchymal NE concentration decreased significantly compared with the left kidney after intervention (average reduction: 40 %, P = 0.0016). Histologic examination revealed apparent denervation with no other vascular or parenchymal injuries observed in the histological and imaging studies.ConclusionEffective and feasible RSD was achieved using CT-guided periarterial ethanol injection. This technique may be a potential alternative to catheter-based RFA in the treatment of hypertension.

  4. 肾交感神经消融对快速起搏心衰犬左室收缩功能的保护作用研究%Study on protective effect of renal sympathetic nerve ablation on the systolic function of left ventricular during the pro- gression of heart failure in dogs

    Institute of Scientific and Technical Information of China (English)

    徐晓宇; 谭晓东

    2015-01-01

    Objective To investigate whether renal sympathetic nerve ablation can protect the systolic function of left ventricular (LV) during the progression of heart failure (HF). Methods 19 beagle dogs were randomly divided into three groups:sham-operated group (n=6), control group (n=7) and ablation group (n=6). Sham-operated group were implanted with pacemakers without pacing. Control group were implanted with pacemakers and underwent 3 weeks of rapid right ventricular pacing, and ablation group bilateral renal sympathetic nerve ablation first, at the same time implanted with pacemakers. 3 days after the rapid right ventricular pacing. Left ventricular strain were analyzed by two-dimensional speckle traching imaging Re-sults After 3 weeks, all the dogs in the control group and ablation group showed greater LV end-diastolic volume compared with the sham-operated group, however, the dogs in the ablation group had a higher LV ejection fraction (LVEF) than the con-trol group (P<0.05). The LV systolic strains were higher in the ablation group than in the control group (P<0.05) for longitudi-nal, circumferential and radial strain, respectively. Conclusion Renal sympathetic nerve ablation can protect the systolic function of left ventricular during the progression of heart failure in dogs.%目的:观察肾交感神经消融是否可以保护心衰犬左室收缩功能。方法19只比格犬随机分为3组:假手术组(n=6)、对照组(n=7)和消融组(n=6)。假手术组犬装起搏器,但不开启;对照组装好起搏器后开始快速右室起搏3周;消融组先对双侧肾交感神经消融,同时植入起搏器,3d后开启快速右室起搏。左室应变通过超声二维斑点追踪技术来评价。结果3周后,对照组和消融组犬左室舒张末期容积较假手术组大;但是,消融组犬左室射血分数高于对照组(P<0.05)。长径方向、圆周方向和径向方向上左室收缩期应变消

  5. Efficacy of regional renal nerve blockade in patients with chronic refractory heart failure

    Institute of Scientific and Technical Information of China (English)

    DAI Qi-ming; FEN Yi; LU Jing; MA Gen-shan

    2013-01-01

    Background Increased renal sympathetic nerve activity can result in diuretic resistance in patients with chronic congestive heart failure.We investigated the effect of regional renal nerve blockade on the patients with chronic refractory heart failure and diuretic resistance.Methods Eighteen patients with chronic refractory heart failure were enrolled (mean age (64±11) years).The patients were randomly divided into two groups (renal nerve blockade group and standard therapy group,n=9 each).Renal nerve blockade was performed by percutaneous injection of local anaesthetic under computed tomographic guidance.Heart rate,mean arterial blood pressure,plasma and urine electrolytes,neurohormones,factional excretion of sodium (FENa),24-hour urine volume were monitored at baseline and the first 24 hours after therapy.Dyspnea and oedema were also evaluated.The major adverse cardiovascular events (MACE),plasma brain natriuretic peptide (BNP) level and left ventricular ejection fraction (LVEF) were compared between the two groups during the 3-12 months follow-up period.Results No complication was observed during the acute phase of renal nerve blockade.After renal nerve blockade,the 24-hour urine volume and FENa were significantly increased,while the level of plasma rennin,angiotensin Ⅱ,aldosterone,BNP and atrial natriuretic peptide as well as dyspnea and oedema were significantly reduced in renal nerve blockade group compared with baseline and standard therapy group.During three to 12 months of follow-up,the rate of MACE and plasma BNP level were significantly lower,while LVEF was significantly higher in renal nerve blockade group than those in standard therapy group.Conclusion Regional renal nerve blockade may be a safe and effective treatment for patients with chronic refractory heart failure.

  6. Sustained sympathetic and blood pressure reduction 1 year after renal denervation in patients with resistant hypertension.

    Science.gov (United States)

    Hering, Dagmara; Marusic, Petra; Walton, Antony S; Lambert, Elisabeth A; Krum, Henry; Narkiewicz, Krzysztof; Lambert, Gavin W; Esler, Murray D; Schlaich, Markus P

    2014-07-01

    Renal denervation (RDN) reduces muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in resistant hypertension. Although a persistent BP-lowering effect has been demonstrated, the long-term effect on MSNA remains elusive. We investigated whether RDN influences MSNA over time. Office BP and MSNA were obtained at baseline, 3, 6, and 12 months after RDN in 35 patients with resistant hypertension. Office BP averaged 166±22/88±19 mm Hg, despite the use of an average of 4.8±2.1 antihypertensive drugs. Baseline MSNA was 51±11 bursts/min ≈2- to 3-fold higher than the level observed in healthy controls. Mean office systolic and diastolic BP significantly decreased by -12.6±18.3/-6.5±9.2, -16.1±25.6/-8.6±12.9, and -21.2±29.1/-11.1±12.9 mm Hg (Phypertension and high baseline MSNA. These observations are compatible with the hypothesis of a substantial contribution of afferent renal nerve signaling to increased BP in resistant hypertension and argue against a relevant reinnervation at 1 year after procedure.

  7. Assessment of cardiac sympathetic nerve integrity with positron emission tomography

    Energy Technology Data Exchange (ETDEWEB)

    Raffel, David M. E-mail: raffel@umich.edu; Wieland, Donald M

    2001-07-01

    The autonomic nervous system plays a critical role in the regulation of cardiac function. Abnormalities of cardiac innervation have been implicated in the pathophysiology of many heart diseases, including sudden cardiac death and congestive heart failure. In an effort to provide clinicians with the ability to regionally map cardiac innervation, several radiotracers for imaging cardiac sympathetic neurons have been developed. This paper reviews the development of neuronal imaging agents and discusses their emerging role in the noninvasive assessment of cardiac sympathetic innervation.

  8. Regulation of bile duct motility by vagus and sympathetic nerves in the pigeon.

    Directory of Open Access Journals (Sweden)

    Neya,Toshiaki

    1990-04-01

    Full Text Available Effects of stimulation of the vagus and sympathetic nerves on bile duct peristalses were studied in pigeons anesthetized with urethane. Vagus stimulation increased the frequency of peristalses. Atropine, hexamethonium and tetrodotoxin abolished this excitatory effect. After atropine, inhibition of peristalses sensitive to tetrodotoxin was produced. Stimulation of sympathetic area in the spinal cord inhibited peristalses. Propranolol converted this effect into an excitatory one, which was abolished by phentolamine. The results suggest that vagal and sympathetic innervations of the bile duct in pigeons are similar to those of the sphincter of Oddi in mammalian species.

  9. Respiratory modulation of sympathetic nerve activity is enhanced in male rat offspring following uteroplacental insufficiency.

    Science.gov (United States)

    Menuet, C; Wlodek, M E; Fong, A Y; Allen, A M

    2016-06-01

    Sympathetic nerve activity to the cardiovascular system displays prominent respiratory-related modulation which leads to the generation of rhythmic oscillations in blood pressure called Traube-Hering waves. An amplification of this respiratory modulation of sympathetic activity is observed in hypertension of both genetic, the spontaneously hypertensive rat, and induced, chronic intermittent hypoxia or maternal protein restriction during gestation, origin. Male offspring of mothers with uteroplacental insufficiency, induced by bilateral uterine vessel ligation at 18 days of gestation, are also hypertensive in adulthood. In this study we examined whether these male offspring display altered respiratory modulation of sympathetic activity at pre-hypertensive ages compared to controls. Respiratory, cardiovascular and sympathetic parameters were examined using the working heart-brainstem preparation in 35 day old male rats that had reduced birth weight due to uteroplacental insufficiency. Whilst all respiratory parameters were not different between groups, we observed an enhanced respiratory-related burst of thoracic sympathetic nerve activity and amplified Traube-Hering waves in the growth-restricted group. This group also showed an increased sympathetic and bradycardic response to activation of peripheral chemoreceptors. The observations add support to the view that altered respiratory modulation of sympathetic activity represents a common mechanism involved in the development of several forms of hypertension.

  10. The role of renal nerve ablation for the management of resistant hypertension and other disease conditions: benefits and concerns.

    Science.gov (United States)

    Faselis, C; Doumas, M; Kokkinos, P; Tsioufis, C; Papademetriou, V

    2014-01-01

    The sympathetic nervous system is overactivated in resistant hypertension and several other disease conditions. A reciprocal association between the brain and the kidney has been described, in that sympathetic overactivity affects renal function while renal injury stimulates central sympathetic drive. Renal nerve ablation has been recently introduced as a potential alternative for the management of resistant hypertension, mainly due to current limitations in pharmacologic antihypertensive therapy. Data accumulated thus far point towards an efficacious and safe interventional method for the management of treatment resistance, with additional benefits on glucose metabolism and cardiac structure and function. Furthermore, beneficial effects have been observed in patients with chronic kidney disease, obstructive sleep apnea, polycystic ovary syndrome, and sympathetically driven tachyarrhythmias. However, as with every novel technique, several questions need to be answered and concerns need to be addressed before the wide application of this interventional approach.

  11. [Sympathetically maintained pain (SMP): phentolamine test vs sympathetic nerve blockade. Comparison of two diagnostic methods].

    Science.gov (United States)

    Wehnert, Y; Müller, B; Larsen, B; Kohn, D

    2002-11-01

    The objective of our study was to clarify whether the phentolamine test is as suitable as sympathetic blockade in diagnosing cases of sympathetically maintained pain. The specificity and the sensitivity of both procedures were examined within a prospective and randomized study. Both a local sympathetic blockade and an intravenous phentolamine infusion were carried out in 29 patients with persistent pain in the area of the upper or lower extremities. A significant improvement was defined as reduction of pain of at least 50%. There were no complications in either test procedure. The phentolamine test registers sympathetically maintained pain well when it has a positive result (specificity of 83%). However, the phentolamine test shows only a low sensitivity of 69%. The phentolamine test, on the other hand, can be realized very easily and safely. Therefore, based on the results obtained, it is recommended that the phentolamine test be applied for primary diagnosis. In case of a negative result, further diagnosis should follow subsequently, for example with local sympathetic blockade.

  12. What can we learn about neural control of the cardiovascular system by studying rhythms in sympathetic nerve activity?

    Science.gov (United States)

    Barman, Susan M

    2016-05-01

    Since the first recordings of sympathetic nerve activity in the 1930s, it was very clear that the activity was organized into bursts synchronized to the respiratory and cardiac cycles. Since the early studies, evidence has accumulated showing that sympathetic neural networks are quite complex and generate a variety of periodicities that range between ~0.04 and 10Hz, depending on the physiological state, type of nerve being analyzed, age of the subject, and the species. Despite the ubiquity of sympathetic rhythms, many investigators have failed to consider this oscillatory characteristic of sympathetic nerve activity and instead rely on simply quantifying changes in the level of activity to make decisions about the role of the sympathetic nervous system in mediating certain behaviors. This review highlights work that shows the importance of including an assessment of the frequency characteristics of sympathetic nerve activity. Copyright © 2015 Elsevier B.V. All rights reserved.

  13. Involvement of hypothalamic AMP-activated protein kinase in leptin-induced sympathetic nerve activation.

    Directory of Open Access Journals (Sweden)

    Mamoru Tanida

    Full Text Available In mammals, leptin released from the white adipose tissue acts on the central nervous system to control feeding behavior, cardiovascular function, and energy metabolism. Central leptin activates sympathetic nerves that innervate the kidney, adipose tissue, and some abdominal organs in rats. AMP-activated protein kinase (AMPK is essential in the intracellular signaling pathway involving the activation of leptin receptors (ObRb. We investigated the potential of AMPKα2 in the sympathetic effects of leptin using in vivo siRNA injection to knockdown AMPKα2 in rats, to produce reduced hypothalamic AMPKα2 expression. Leptin effects on body weight, food intake, and blood FFA levels were eliminated in AMPKα2 siRNA-treated rats. Leptin-evoked enhancements of the sympathetic nerve outflows to the kidney, brown and white adipose tissues were attenuated in AMPKα2 siRNA-treated rats. To check whether AMPKα2 was specific to sympathetic changes induced by leptin, we examined the effects of injecting MT-II, a melanocortin-3 and -4 receptor agonist, on the sympathetic nerve outflows to the kidney and adipose tissue. MT-II-induced sympatho-excitation in the kidney was unchanged in AMPKα2 siRNA-treated rats. However, responses of neural activities involving adipose tissue to MT-II were attenuated in AMPKα2 siRNA-treated rats. These results suggest that hypothalamic AMPKα2 is involved not only in appetite and body weight regulation but also in the regulation of sympathetic nerve discharges to the kidney and adipose tissue. Thus, AMPK might function not only as an energy sensor, but as a key molecule in the cardiovascular, thermogenic, and lipolytic effects of leptin through the sympathetic nervous system.

  14. Involvement of hypothalamic AMP-activated protein kinase in leptin-induced sympathetic nerve activation.

    Science.gov (United States)

    Tanida, Mamoru; Yamamoto, Naoki; Shibamoto, Toshishige; Rahmouni, Kamal

    2013-01-01

    In mammals, leptin released from the white adipose tissue acts on the central nervous system to control feeding behavior, cardiovascular function, and energy metabolism. Central leptin activates sympathetic nerves that innervate the kidney, adipose tissue, and some abdominal organs in rats. AMP-activated protein kinase (AMPK) is essential in the intracellular signaling pathway involving the activation of leptin receptors (ObRb). We investigated the potential of AMPKα2 in the sympathetic effects of leptin using in vivo siRNA injection to knockdown AMPKα2 in rats, to produce reduced hypothalamic AMPKα2 expression. Leptin effects on body weight, food intake, and blood FFA levels were eliminated in AMPKα2 siRNA-treated rats. Leptin-evoked enhancements of the sympathetic nerve outflows to the kidney, brown and white adipose tissues were attenuated in AMPKα2 siRNA-treated rats. To check whether AMPKα2 was specific to sympathetic changes induced by leptin, we examined the effects of injecting MT-II, a melanocortin-3 and -4 receptor agonist, on the sympathetic nerve outflows to the kidney and adipose tissue. MT-II-induced sympatho-excitation in the kidney was unchanged in AMPKα2 siRNA-treated rats. However, responses of neural activities involving adipose tissue to MT-II were attenuated in AMPKα2 siRNA-treated rats. These results suggest that hypothalamic AMPKα2 is involved not only in appetite and body weight regulation but also in the regulation of sympathetic nerve discharges to the kidney and adipose tissue. Thus, AMPK might function not only as an energy sensor, but as a key molecule in the cardiovascular, thermogenic, and lipolytic effects of leptin through the sympathetic nervous system.

  15. The sympathetic nervous system in obesity hypertension.

    Science.gov (United States)

    Lohmeier, Thomas E; Iliescu, Radu

    2013-08-01

    Abundant evidence supports a role of the sympathetic nervous system in the pathogenesis of obesity-related hypertension. However, the nature and temporal progression of mechanisms underlying this sympathetically mediated hypertension are incompletely understood. Recent technological advances allowing direct recordings of renal sympathetic nerve activity (RSNA) in conscious animals, together with direct suppression of RSNA by renal denervation and reflex-mediated global sympathetic inhibition in experimental animals and human subjects have been especially valuable in elucidating these mechanisms. These studies strongly support the concept that increased RSNA is the critical mechanism by which increased central sympathetic outflow initiates and maintains reductions in renal excretory function, causing obesity hypertension. Potential determinants of renal sympathoexcitation and the differential mechanisms mediating the effects of renal-specific versus reflex-mediated, global sympathetic inhibition on renal hemodynamics and cardiac autonomic function are discussed. These differential mechanisms may impact the efficacy of current device-based approaches for hypertension therapy.

  16. Heart Rate Changes in Response to Mechanical Pressure Stimulation of Skeletal Muscles Are Mediated by Cardiac Sympathetic Nerve Activity

    Science.gov (United States)

    Watanabe, Nobuhiro; Hotta, Harumi

    2017-01-01

    Stimulation of mechanoreceptors in skeletal muscles such as contraction and stretch elicits reflexive autonomic nervous system changes which impact cardiovascular control. There are pressure-sensitive mechanoreceptors in skeletal muscles. Mechanical pressure stimulation of skeletal muscles can induce reflex changes in heart rate (HR) and blood pressure, although the neural mechanisms underlying this effect are unclear. We examined the contribution of cardiac autonomic nerves to HR responses induced by mechanical pressure stimulation (30 s, ~10 N/cm2) of calf muscles in isoflurane-anesthetized rats. Animals were artificially ventilated and kept warm using a heating pad and lamp, and respiration and core body temperature were maintained within physiological ranges. Mechanical stimulation was applied using a stimulation probe 6 mm in diameter with a flat surface. Cardiac sympathetic and vagus nerves were blocked to test the contribution of the autonomic nerves. For sympathetic nerve block, bilateral stellate ganglia, and cervical sympathetic nerves were surgically sectioned, and for vagus nerve block, the nerve was bilaterally severed. In addition, mass discharges of cardiac sympathetic efferent nerve were electrophysiologically recorded. Mechanical stimulation increased or decreased HR in autonomic nerve-intact rats (range: −56 to +10 bpm), and the responses were negatively correlated with pre-stimulus HR (r = −0.65, p = 0.001). Stimulation-induced HR responses were markedly attenuated by blocking the cardiac sympathetic nerve (range: −9 to +3 bpm, p mechanical stimulation increased, or decreased the frequency of sympathetic nerve activity in parallel with HR (r = 0.77, p = 0.0004). Furthermore, the changes in sympathetic nerve activity were negatively correlated with its tonic level (r = −0.62, p = 0.0066). These results suggest that cardiac sympathetic nerve activity regulates HR responses to muscle mechanical pressure stimulation and the direction of HR

  17. Renal sympathetic denervation for treatment of patients with heart failure: summary of the available evidence.

    Science.gov (United States)

    Nammas, Wail; Koistinen, Juhani; Paana, Tuomas; Karjalainen, Pasi P

    2017-02-10

    Heart failure syndrome results from compensatory mechanisms that operate to restore - back to normal - the systemic perfusion pressure. Sympathetic overactivity plays a pivotal role in heart failure; norepinephrine contributes to maintenance of the systemic blood pressure and increasing preload. Cardiac norepinephrine spillover increases in patients with heart failure; norepinephrine exerts direct toxicity on cardiac myocytes resulting in a decrease of synthetic activity and/or viability. Importantly, cardiac norepinephrine spillover is a powerful predictor of mortality in patients with moderate to severe HF. This provided the rationale for trials that demonstrated survival benefit associated with the use of beta adrenergic blockers in heart failure with reduced ejection fraction. Nevertheless, the MOXCON trial demonstrated that rapid uptitration of moxonidine (inhibitor of central sympathetic outflow) in patients with heart failure was associated with excess mortality and morbidity, despite reduction of plasma norepinephrine. Interestingly, renal norepinephrine spillover was the only independent predictor of adverse outcome in patients with heart failure, in multivariable analysis. Recently, renal sympathetic denervation has emerged as a novel approach for control of blood pressure in patients with treatment-resistant hypertension. This article summarizes the available evidence for the effect of renal sympathetic denervation in the setting of heart failure. Key messages Experimental studies supported a beneficial effect of renal sympathetic denervation in heart failure with reduced ejection fraction. Clinical studies demonstrated improvement of symptoms, and left ventricular function. In heart failure and preserved ejection fraction, renal sympathetic denervation is associated with improvement of surrogate endpoints.

  18. Effects of dexamethasone on estrogen- and pregnancy-induced plasticity in rat uterine sympathetic nerves.

    Science.gov (United States)

    Bianchimano, P; Frías, A I; Richeri, A; Brauer, M M

    2007-12-01

    Estrogen and glucocorticoids are known to evoke opposing effects on the uterus. We analyzed the effects of dexamethasone (DEX) on uterine sympathetic denervation elicited by short- and long-term exposure to estrogen of intact prepubertal rats. We also studied the effects of DEX on the physiological degeneration of uterine sympathetic nerves at term pregnancy. Changes in innervation were assessed quantitatively by using computer-assisted methods on uterine cryostat tissue sections stained for tyrosine hydroxylase. At 24 h following treatment of prepubertal rats (25 days of age) with 1 microg or 2.5 microg estrogen, marked increases in uterine size and reductions in the percentage nerve area were observed. Co-administration of DEX (4 mg/kg) attenuated both these short-term estrogen-induced effects. Treatment of 19-day-old rats with a single dose of 25 mug estrogen provoked, at 26 days of age, a 54% reduction in the total nerve area. This reduction was abolished by the co-administration of nine doses of DEX (0.5 mg/kg) at 18-26 days of age. Treatment of rats with the same regime of DEX alone increased the total nerve area by 46% of the control values. Studies of control pregnant rats revealed the unexpected presence of intrauterine nerve fibers at term. Treatment of pregnant rats with six doses of DEX (4 mg/kg) at 16-21 days of age had no effects on the density of uterine sympathetic nerves. These results suggest that DEX has growth-promoting effects on immature uterine sympathetic nerves and may antagonize the degenerative effects elicited by long-term exposure to estrogen.

  19. Cardiorenal axis and arrhythmias: Will renal sympathetic denervation provide additive value to the therapeutic arsenal?

    Science.gov (United States)

    van Brussel, Peter M; Lieve, Krystien V V; de Winter, Robbert J; Wilde, Arthur A M

    2015-05-01

    Disruption of sympathetic tone may result in the occurrence or maintenance of cardiac arrhythmias. Multiple arrhythmic therapies that intervene by influencing cardiac sympathetic tone are common in clinical practice. These vary from pharmaceutical (β-blockers, angiotensin-converting enzyme inhibitors, and calcium antagonists) to percutaneous/surgical (cardiac sympathetic denervation) interventions. In some patients, however, these therapies have insufficient prophylactic and therapeutic capabilities. A safe and effective additional therapy wherein sympathetic drive is further attenuated would be expedient. Recently, renal sympathetic denervation (RSD) has been subject of research for various sympathetic nervous system-related diseases. By its presumed afferent and efferent sympatholytic effects, RSD might indirectly attenuate sympathetic outflow via the brain to the heart but might also reduce systemic catecholamine excretion and might therefore reduce catecholamine-sensitive arrhythmias. RSD is subject of research for various sympathetically driven arrhythmias, both supraventricular and ventricular. In this review, we give an overview of the rationale behind RSD as potential therapy in mediating arrhythmias that are triggered by a disrupted sympathetic nervous system and discuss the presently available results from animal and human studies.

  20. The syndrome of renal tubular acidosis with nerve deafness.

    Science.gov (United States)

    Donckerwolcke, R A; Van Biervliet, J P; Koorevaar, G; Kuijten, R H; Van Stekelenburg, G J

    1976-01-01

    Two brothers with renal tubular acidosis and nerve deafness are described. Studies of the physiopathological characteristics of the renal acidification defect show that the defect is limited to the distal tubule. Renal tubular acidosis with nerve deafness is a distinct nosologic entity that is determined by an autosomal recessive trait.

  1. THE CAFETERIA DIET INCREASES FAT MASS AND CHRONICALLY ELEVATES LUMBAR SYMPATHETIC NERVE ACTIVITY IN RATS

    Science.gov (United States)

    Muntzel, Martin S.; Al-Naimi, Omar Ali S.; Barclay, Alicia; Ajasin, David

    2012-01-01

    Obesity causes sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Because high-fat induced weight gain in rats elevates plasma leptin at 1–3 days following onset of calorie dense diets, we hypothesized that diet-induced overfeeding will increase sympathetic activity within one week following onset of the regimen. To test this, we continuously measured sympathetic activity and blood pressure before and during the onset of diet-induced obesity using a high calorie cafeteria-style diet. Female Wistar rats, in which radiotelemeters had been implanted for continuous monitoring of lumbar sympathetic activity, mean arterial pressure, and heart rate, were randomly assigned to groups that received regular chow (control) or a cafeteria diet for a period of 15 days. This short-term cafeteria-feeding regimen caused modest but non-significant increases in body weight (P = 0.07) and a doubling of brown and white adipose tissue (P cafeteria rats compared with controls (P Cafeteria diet-induced weight gain caused increases in lumbar sympathetic nerve activity that became significant by the 12th day of the diet (p cafeteria-style diet stimulates sustained increases in lumbar sympathetic neural drive in rats. PMID:23090774

  2. Cafeteria diet increases fat mass and chronically elevates lumbar sympathetic nerve activity in rats.

    Science.gov (United States)

    Muntzel, Martin S; Al-Naimi, Omar Ali S; Barclay, Alicia; Ajasin, David

    2012-12-01

    Obesity causes sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Because high-fat induced weight gain in rats elevates plasma leptin at 1 to 3 days after the onset of calorie-dense diets, we hypothesized that diet-induced overfeeding will increase sympathetic activity within 1 week after the onset of the regimen. To test this, we continuously measured sympathetic activity and blood pressure before and during the onset of diet-induced obesity using a high-calorie, cafeteria-style diet. Female Wistar rats, in which radiotelemeters had been implanted for continuous monitoring of lumbar sympathetic activity, mean arterial pressure, and heart rate, were randomly assigned to groups that received regular chow (control) or a cafeteria diet for a period of 15 days. This short-term, cafeteria-feeding regimen caused modest but nonsignificant increases in body weight (P=0.07) and a doubling of brown and white adipose tissue (Pcafeteria rats compared with controls (PCafeteria diet-induced weight gain caused increases in lumbar sympathetic nerve activity that became significant by the 12th day of the diet (Pcafeteria-style diet stimulates sustained increases in lumbar sympathetic neural drive in rats.

  3. Recovery of sympathetic nerve function after lumbar sympathectomy is slower in the hind limbs than in the torso.

    Science.gov (United States)

    Zheng, Zhi-Fang; Liu, Yi-Shu; Min, Xuan; Tang, Jian-Bing; Liu, Hong-Wei; Cheng, Biao

    2017-07-01

    Local sympathetic denervation by surgical sympathectomy is used in the treatment of lower limb ulcers and ischemia, but the restoration of cutaneous sympathetic nerve functions is less clear. This study aims to explore the recovery of cutaneous sympathetic functions after bilateral L2-4 sympathectomy. The skin temperature of the left feet, using a point monitoring thermometer, increased intraoperatively after sympathectomy. The cytoplasm of sympathetic neurons contained tyrosine hydroxylase and dopamine β-hydroxylase, visualized by immunofluorescence, indicated the accuracy of sympathectomy. Iodine starch test results suggested that the sweating function of the hind feet plantar skin decreased 2 and 7 weeks after lumbar sympathectomy but had recovered by 3 months. Immunofluorescence and western blot assay results revealed that norepinephrine and dopamine β-hydroxylase expression in the skin from the sacrococcygeal region and hind feet decreased in the sympathectomized group at 2 weeks. Transmission electron microscopy results showed that perinuclear space and axon demyelination in sympathetic cells in the L5 sympathetic trunks were found in the sympathectomized group 3 months after sympathectomy. Although sympathetic denervation occurred in the sacrococcygeal region and hind feet skin 2 weeks after lumbar sympathectomy, the skin functions recovered gradually over 7 weeks to 3 months. In conclusion, sympathetic functional recovery may account for the recurrence of hyperhidrosis after sympathectomy and the normalization of sympathetic nerve trunks after incomplete injury. The recovery of sympathetic nerve function was slower in the limbs than in the torso after bilateral L2-4 sympathectomy.

  4. Co-localization of histamine and norepinephrine in sympathetic ganglia and exocytosis of endogenous histamine from cardiac sympathetic nerve endings of macaca mulatto monkey

    Institute of Scientific and Technical Information of China (English)

    Ming-kaiLI; Xiao-xingLUO; Liang-weiCHEN; ZhongCHEN; JiaMENG; JingHU; Yu-meiWU; Jing-ruMENG; ZhengHOU; XueMA

    2005-01-01

    AIM To provide the evidence about localization, biosynthesis, metabolism and release of histamine from the cardiac sympathetic nerve terminals, and endogenous sympathetic histamine could inhibit itsel frelease from the nerve terminal through the presynaptic histamine H3 receptor. METHODS Using double-labeled immunohistochemistry to observe the co-localization of histamine and NE in the superior cer-vical ganglia (SCG) of macaca mulatto monkey; Different-speed centrifugation to obtain the cardiac sympathetic nerve terminal model (the cardiac synaptosomes), spectrofluorometer and ELISA techniques to detect the release of histamine from the cardiacsynaptosomes. RESULTS ( 1 ) The coexistence of histamine and norepinephrine immunoreactivities was identified in the same neuron within SCG of macaca mulatto monkey. (2) Depolarization of macaca mulatto monkey cardiac synaptosomes with 50 mmol/L potassium caused the release of endogenous histamine,

  5. DMPP-evoked increases in postganglionic sympathetic nerve activity and blood pressure occurs by two mechanisms in the rat.

    Science.gov (United States)

    Martin, J R

    1997-08-01

    1. Intravenous administration of the ganglionic nicotinic receptor agonist DMPP (1,1-dimethyl-4-phenylpiperazinium iodide) into urethane-anaesthetized rats evoked dose-dependent increases in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). 2. The ganglionic nicotinic receptor antagonists pentolinium and hexamethonium either alone or combined did not inhibit the increase in RSNA and MAP evoked by 50 to 200 micrograms kg-1 doses of DMPP. The increase in renal sympathetic nerve activity evoked by DMPP occurred as a brief burst in firing. 3. The increase in MAP, but not RSNA, evoked by DMPP in the presence of pentolinium was inhibited by the selective alpha 1-adrenergic receptor antagonist prazosin. 4. The non-selective alpha-adrenoceptor and NPY receptor antagonist benextramine also inhibited the increase in MAP without inhibiting the increase in RSNA. Surprisingly, the combination of benextramine and pentolinium, or benextramine and hexamethonium, completely blocked the DMPP-evoked increase in RSNA and thus the increase in MAP. 5. The uptake1 antagonist desipramine combined with pentolinium did not affect the DMPP-evoked increases in MAP or RSNA when compared to the responses evoked in the presence of pentolinium alone. 6. Adding the selective M1 muscarinic receptor antagonist telenzepine to pentolinium and prazosin did not inhibit the increase in RSNA evoked by a 100 micrograms kg-1 dose of DMPP. 7. While the DMPP-evoked increase in MAP in the presence of ganglionic nicotinic receptor antagonists is primarily dependent upon activation of alpha 1-adrenoceptors, the increase in RSNA occurs via activation of ganglionic nicotinic receptors and activation of a mechanism susceptible to blockade by benextramine.

  6. Change in sympathetic nerve firing pattern associated with dietary weight loss in the metabolic syndrome

    Directory of Open Access Journals (Sweden)

    Elisabeth Annie Lambert

    2011-08-01

    Full Text Available Sympathetic activation in subjects with the metabolic syndrome (MS plays a role in the pathogenesis of cardiovascular disease development. Diet-induced weight loss decreases sympathetic outflow. However the mechanisms that account for sympathetic inhibition are not known. We sought to provide a detailed description of the sympathetic response to diet by analyzing the firing behavior of single-unit sympathetic nerve fibres. Fourteen subjects (57±2 years, 9 men, 5 females fulfilling ATP III criteria for the MS underwent a 3-month low calorie diet. Metabolic profile, hemodynamic parameters and multi-unit and single unit muscle sympathetic nerve activity (MSNA, microneurography were assessed prior to and at the end of the diet. Patients’ weight dropped from 96±4 to 88±3 kg (P<0.001. This was associated with a decrease in systolic and diastolic blood pressure (-12 ±3 and -5±2 mmHg, P<0.05, and in heart rate (-7±2 bpm, P<0.01 and an improvement in all metabolic parameters (fasting glucose: -0.302.1±0.118 mmol/l, total cholesterol: -0.564±0.164 mmol/l, triglycerides: -0.414±0.137 mmol/l, P<0.05. Multi-unit MSNA decreased from 68±4 to 59±5 bursts per 100 heartbeats (P<0.05. Single-unit MSNA indicated that the firing rate of individual vasoconstrictor fibres decreased from 59±10 to 32±4 spikes per 100 heart beats (P<0.05. The probability of firing decreased from 34±5 to 23±3 % of heartbeats (P<0.05, and the incidence of multiple firing decreased from 14±4 to 6±1 % of heartbeats (P<0.05. Cardiac and sympathetic baroreflex function were significantly improved (cardiac slope: 6.57±0.69 to 9.57±1.20 msec.mmHg-1; sympathetic slope: -3.86±0.34 to -5.05±0.47 bursts per 100 heartbeats.mmHg-1 P<0.05 for both. Hypocaloric diet decreased sympathetic activity and improved hemodynamic and metabolic parameters. The sympathoinhibition associated with weight loss involves marked changes, not only in the rate but also in the firing pattern of

  7. Effects of deep and superficial experimentally induced acute pain on muscle sympathetic nerve activity in human subjects

    National Research Council Canada - National Science Library

    A. R. Burton; I. Birznieks; P. S. Bolton; L. A. Henderson; V. G. Macefield

    2009-01-01

    ...), whereas deep pain is believed to cause vasodepression. To date, no studies have addressed whether deep or superficial pain produces such differential effects on muscle sympathetic nerve activity (MSNA...

  8. Cilnidipine suppresses cardiac sympathetic nerve activation induced-electical stimulation in canine blood-perfused papillary muscle preparation

    National Research Council Canada - National Science Library

    Kazuyuki Daitoku; Kazuhiko Seya; Shigeru Motomura

    1999-01-01

    ...) and the NE release in the same preparation. When the intracardiac sympathetic nerves were electricaly stimulated by the field stimulation through silver electrode which was attached to the base of PM, the DT and NE release were voltage...

  9. Acute electromyostimulation decreases muscle sympathetic nerve activity in patients with advanced chronic heart failure (EMSICA Study.

    Directory of Open Access Journals (Sweden)

    Marc Labrunée

    Full Text Available BACKGROUND: Muscle passive contraction of lower limb by neuromuscular electrostimulation (NMES is frequently used in chronic heart failure (CHF patients but no data are available concerning its action on sympathetic activity. However, Transcutaneous Electrical Nerve Stimulation (TENS is able to improve baroreflex in CHF. The primary aim of the present study was to investigate the acute effect of TENS and NMES compared to Sham stimulation on sympathetic overactivity as assessed by Muscle Sympathetic Nerve Activity (MSNA. METHODS: We performed a serie of two parallel, randomized, double blinded and sham controlled protocols in twenty-two CHF patients in New York Heart Association (NYHA Class III. Half of them performed stimulation by TENS, and the others tested NMES. RESULTS: Compare to Sham stimulation, both TENS and NMES are able to reduce MSNA (63.5 ± 3.5 vs 69.7 ± 3.1 bursts / min, p < 0.01 after TENS and 51.6 ± 3.3 vs 56.7 ± 3.3 bursts / min, p < 0, 01 after NMES. No variation of blood pressure, heart rate or respiratory parameters was observed after stimulation. CONCLUSION: The results suggest that sensory stimulation of lower limbs by electrical device, either TENS or NMES, could inhibit sympathetic outflow directed to legs in CHF patients. These properties could benefits CHF patients and pave the way for a new non-pharmacological approach of CHF.

  10. Involvement of the histaminergic system in renal sympathetic and cardiovascular responses to leptin and ghrelin.

    Science.gov (United States)

    Tanida, Mamoru; Kaneko, Hidekazu; Shen, Jiao; Nagai, Katsuya

    2007-02-01

    Previous studies have demonstrated that histamine affects blood pressure (BP) in anesthetized rats. Here, we examined the effects of lateral cerebral ventricular (LCV) injection of various doses of histamine on renal sympathetic nerve activity (RSNA) and BP in anesthetized rats. LCV injection of a low dose of histamine (0.0001nmol) suppressed RSNA and BP. Conversely, a high dose of histamine (100nmol) elevated both RSNA and BP. Moreover, inhibiting effects of a low dose of histamine were eliminated by LCV pre-injection of thioperamide, an antagonist of histaminergic H3-receptor, and accelerating effects of a high dose of histamine were abolished by LCV pre-injection of diphenhydramine, an antagonist of histaminergic H1-receptor. Thus, these evidences suggest that central histamine affects RSNA and BP via histaminergic receptors. In addition, we examined a role for histaminergic system in cardiovascular modulators such as leptin and ghrelin. The LCV pre-injection of thioperamide clearly blocked suppressing effects of ghrelin on RSNA and BP. The LCV pre-injection of diphenhydramine also blocked elevating effects of leptin. Therefore, these results suggest that leptin and ghrelin might affect RSNA and BP by mediating central histaminegic H1- and H3-receptors, respectively.

  11. Hypothalamic Paraventricular and Arcuate Nuclei Contribute to Elevated Sympathetic Nerve Activity in Pregnant Rats: Roles of Neuropeptide Y and α-Melanocyte-Stimulating Hormone.

    Science.gov (United States)

    Shi, Zhigang; Cassaglia, Priscila A; Gotthardt, Laura C; Brooks, Virginia L

    2015-12-01

    Pregnancy increases sympathetic nerve activity (SNA), but the mechanisms are unknown. Here, we investigated the contributions of the hypothalamic paraventricular and arcuate nuclei in α-chloralose-anesthetized pregnant and nonpregnant rats. Baseline arterial pressure (AP) was lower, and heart rate (HR), lumbar sympathetic activity, and splanchnic SNA were higher in pregnant rats compared with nonpregnant rats. Inhibition of the paraventricular nucleus via bilateral muscimol nanoinjections decreased AP and HR more in pregnant rats than in nonpregnant rats and decreased lumbar SNA only in pregnant rats. Similarly, after arcuate muscimol nanoninjections, the decreases in AP, HR, and lumbar, renal, and splanchnic sympathetic nerve activities were greater in pregnant rats than in nonpregnant rats. Major arcuate neuronal groups that project to the paraventricular nucleus express inhibitory neuropeptide Y (NPY) and excitatory α-melanocyte-stimulating hormone. Inhibition of paraventricular melanocortin 3/4 receptors with SHU9119 also decreased AP, HR, and lumbar SNA in pregnant rats but not in nonpregnant rats. Conversely, paraventricular nucleus NPY expression was reduced in pregnant animals, and although blockade of paraventricular NPY Y1 receptors increased AP, HR, and lumbar sympathetic activity in nonpregnant rats, it had no effects in pregnant rats. Yet, the sympathoinhibitory, depressor, and bradycardic effects of paraventricular NPY nanoinjections were similar between groups. In conclusion, the paraventricular and arcuate nuclei contribute to increased basal SNA during pregnancy, likely due in part to decreased tonic NPY inhibition and increased tonic α-melanocyte-stimulating hormone excitation of presympathetic neurons in the paraventricular nucleus.

  12. Marked loss of sympathetic nerve fibers in chronic Charcot foot of diabetic origin compared to ankle joint osteoarthritis.

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    Koeck, Franz-Xaver; Bobrik, Verena; Fassold, Alexander; Grifka, Joachim; Kessler, Sigurd; Straub, Rainer H

    2009-06-01

    The pathogenesis of Charcot foot is based on three disputed factors: (1) loss of neurotrophic influence, (2) microtraumatic lesions, and (3) neurovascular disturbances. These etiological causes were uncovered by clinicophysiological tests. However, no results of quantitative nerve density studies of sympathetic and sensory substance P-positive (SP+) nerve fibers are available. We studied the density of sympathetic and SP+ nerve fibers in three distinct areas of the tarsus. Fifteen patients with ankle osteoarthritis (OA) and 15 patients with diabetic Charcot foot were included. Patients with OA did not differ from those with Charcot foot in SP+ sensory nerve fiber density. However, at all three areas, the density of sympathetic nerve fibers was significantly lower in patients with Charcot foot compared to OA (p = 0.006). In addition, we found that the sympathetic nerve repellent factor semaphorin 3C was highly expressed in inflamed tissue in Charcot patients. In Charcot foot of diabetic origin a severe loss of sympathetic nerve fibers was observed. These findings in chronically inflamed Charcot foot lend support to the neurovascular theory in the late chronic phase, which probably depends on the inflammatory upregulation of nerve repellent factors.

  13. Interactions between nitric oxide and renal nerves on pressure-diuresis and natriuresis.

    Science.gov (United States)

    Madrid, M I; Salom, M G; Tornel, J; López, E; Fenoy, F J

    1998-09-01

    The present study examined the effect of renal denervation on the impairment of the pressure-diuresis response produced by nitric oxide synthesis blockade. The experiments were performed in Inactin-anesthetized Munich-Wistar rats. The animals with innervated kidneys had lower baseline values of renal blood flow, GFR, sodium excretion (UNaV), and urine flow (V) than rats with denervated kidneys. Also, renal denervation shifted pressure-diuresis and natriuresis toward lower pressures. A low dose of N(omega)-nitro-L-arginine methyl esther (NAME, 3.7 nmol/kg per min) reduced UNaV and the fractional excretion of sodium (FENa) and blunted pressure-natriuresis only in rats with innervated kidneys, whereas it had no effects in rats with denervated kidneys. A medium dose of NAME (37 nmol/kg per min) lowered FENa only in rats with innervated kidneys. The administration of NAME (37 nmol/kg per min) blunted pressure-diuresis and natriuresis in kidneys with or without the renal nerves, but the effect was more pronounced in rats with innervated kidneys. A high dose of NAME (3.7 micromol + 185 nmol/kg per min) increased UNaV and FENa only in rats with innervated kidneys, whereas it reduced GFR, V, UnaV, and FENa in rats with denervated kidneys. However, pressure-natriuresis and diuresis were blunted by this high dose of NAME independently of the presence or absence of renal nerves. These results demonstrate that renal nerves potentiate the renal effects of low doses of NAME on renal function and pressure-diuresis and natriuresis. However, high doses of NAME abolish pressure-diuresis independently of renal nerves, and the natriuretic effect of NAME in innervated kidneys may be attributed to reflex inhibition of sympathetic tone due to the rise in arterial pressure.

  14. Functional role of lumbar sympathetic nerves and supraspinal mechanism in the defecation reflex of the cat.

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    Takaki,Miyako

    1987-12-01

    Full Text Available The role of the lumbar sympathetic nerves and supraspinal mechanism in the defecation reflex was investigated in 30 adult cats and 6 kittens. One or two propulsive contractions, whose mean pressure evoked was more than about 90 cmH2O (adult cats and 50 cmH2O (kittens, were induced in the rectum of all animals by rectal distension. These propulsive contractions could be generated at the descending and the transverse colons. The removal of the supraspinal influence by spinal transection at T13 or removal of pelvic afferents to the supraspinal center by spinal transection at L abolished the propulsive contractions. Successive lumbar sympathectomy restored the contractions. Lumbar sympathectomy and the successive removal of the supraspinal influence did not affect the propulsive contractions. In both cases, the final exclusion of the sacral segments by pithing of the spinal cord abolished the propulsive contractions. These results suggest that the sacral excitatory reflex mediated via pelvic nerves and the lumbar inhibitory reflex mediated via lumbar sympathetic nerves can function during rectal distension in spinal cats and that the lumbar inhibitory reflex is suppressed by the supraspinal sympathetic inhibitory reflex activated by pelvic afferents in intact cats, as in guinea pigs, resulting in propulsive contractions.

  15. Cardiac-locked bursts of muscle sympathetic nerve activity are absent in familial dysautonomia.

    Science.gov (United States)

    Macefield, Vaughan G; Norcliffe-Kaufmann, Lucy; Axelrod, Felicia B; Kaufmann, Horacio

    2013-02-01

    Familial dysautonomia (Riley-Day syndrome) is an hereditary sensory and autonomic neuropathy (HSAN type III), expressed at birth, that is associated with reduced pain and temperature sensibilities and absent baroreflexes, causing orthostatic hypotension as well as labile blood pressure that increases markedly during emotional excitement. Given the apparent absence of functional baroreceptor afferents, we tested the hypothesis that the normal cardiac-locked bursts of muscle sympathetic nerve activity (MSNA) are absent in patients with familial dysautonomia. Tungsten microelectrodes were inserted percutaneously into muscle or cutaneous fascicles of the common peroneal nerve in 12 patients with familial dysautonomia. Spontaneous bursts of MSNA were absent in all patients, but in five patients we found evidence of tonically firing sympathetic neurones, with no cardiac rhythmicity, that increased their spontaneous discharge during emotional arousal but not during a manoeuvre that unloads the baroreceptors. Conversely, skin sympathetic nerve activity (SSNA), recorded in four patients, appeared normal. We conclude that the loss of phasic bursts of MSNA and the loss of baroreflex modulation of muscle vasoconstrictor drive contributes to the poor control of blood pressure in familial dysautonomia, and that the increase in tonic firing of muscle vasoconstrictor neurones contributes to the increase in blood pressure during emotional excitement.

  16. Advances in Renal Sympathetic Denervation%肾脏交感神经射频消融术临床效应研究进展

    Institute of Scientific and Technical Information of China (English)

    肖宜超

    2012-01-01

    Renal sympathetic denervation (RSD) is a novel catheter-based approach to directly target renal sympathetic nerves using radiofrequency ablation technology, which can suppress the activation of the sympathetic nervous system. It has been indicated that RSD can not only significantly lower peripheral blood pressure in patients with resistant hypertension, but shows improvement in left ventricular hypertrophy , heart failure, insulin resistance and albuminuria. This review focuses on the clinical effects of renal sympathetic denervation and the prospects of its clinical application.%肾脏交感神经射频消融术是一种新型的、选择性降低肾脏交感神经活性的介入治疗手段,最新研究证实不仅可显著降低顽固性高血压患者血压水平,而且临床研究发现还具有逆转左心室肥厚、改善心功能、改善胰岛素抵抗、降低尿蛋白等临床效应;现主要对肾脏交感神经射频消融术的临床效应及应用前景进行综述.

  17. Effects of renal sympathetic denervation on post-myocardial infarction cardiac remodeling in rats.

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    Jialu Hu

    Full Text Available OBJECTIVE: To investigate the therapeutic effects of renal denervation (RD on post- myocardial infarction (MI cardiac remodeling in rats, the most optimal time for intervention and the sustainability of these effects. METHODS: One hundred SPF male Wistar rats were randomly assigned to N group (Normal, n=10, MI group(MI, n=20,RD group (RD, n=10, RD3+MI (MI three days after RD, n=20, MI1+RD (RD one day after MI, n=20, MI7+RD (RD seven days after MI, n=20. MI was produced through thoracotomic ligation of the anterior descending artery. RD was performed through laparotomic stripping of the renal arteriovenous adventitial sympathetic nerve. Left ventricular function, hemodynamics, plasma BNP, urine volume, urine sodium excretion and other indicators were measured four weeks after MI. RESULTS: (1 The left ventricular function of the MI group significantly declined (EF<40%, plasma BNP was elevated, urine output was significantly reduced, and 24-hour urine sodium excretion was significantly reduced. (2 Denervation can be achieved by surgically stripping the arteriovenous adventitia, approximately 3 mm from the abdominal aorta. (3 In rats with RD3+MI, MI1+RD and MI7+RD, compared with MI rats respectively, the LVEF was significantly improved (75 ± 8.4%,69 ± 3.8%,73 ± 5.5%, hemodynamic indicators were significantly improved, plasma BNP was significantly decreased, and the urine output was significantly increased (21.3 ± 5 ml,23.8 ± 5.4 ml,25.2 ± 8.7 ml. However, the urinary sodium excretion also increased but without significant difference. CONCLUSIONS: RD has preventive and therapeutic effects on post-MI cardiac remodeling.These effects can be sustained for at least four weeks, but there were no significant differences between denervation procedures performed at different times in the course of illness. Cardiac function, hemodynamics, urine volume and urine sodium excretion in normal rats were not affected by RD.

  18. Human muscle sympathetic nerve activity and plasma noradrenaline kinetics in space

    Science.gov (United States)

    Ertl, Andrew C.; Diedrich, Andre; Biaggioni, Italo; Levine, Benjamin D.; Robertson, Rose Marie; Cox, James F.; Zuckerman, Julie H.; Pawelczyk, James A.; Ray, Chester A.; Buckey, Jay C Jr; Lane, Lynda D.; Shiavi, Richard; Gaffney, F. Andrew; Costa, Fernando; Holt, Carol; Blomqvist, C. Gunnar; Eckberg, Dwain L.; Baisch, Friedhelm J.; Robertson, David

    2002-01-01

    Astronauts returning from space have reduced red blood cell masses, hypovolaemia and orthostatic intolerance, marked by greater cardio-acceleration during standing than before spaceflight, and in some, orthostatic hypotension and presyncope. Adaptation of the sympathetic nervous system occurring during spaceflight may be responsible for these postflight alterations. We tested the hypotheses that exposure to microgravity reduces sympathetic neural outflow and impairs sympathetic neural responses to orthostatic stress. We measured heart rate, photoplethysmographic finger arterial pressure, peroneal nerve muscle sympathetic activity and plasma noradrenaline spillover and clearance, in male astronauts before, during (flight day 12 or 13) and after the 16 day Neurolab space shuttle mission. Measurements were made during supine rest and orthostatic stress, as simulated on Earth and in space by 7 min periods of 15 and 30 mmHg lower body suction. Mean (+/- S.E.M.) heart rates before lower body suction were similar pre-flight and in flight. Heart rate responses to -30 mmHg were greater in flight (from 56 +/- 4 to 72 +/- 4 beats min(-1)) than pre-flight (from 56 +/- 4 at rest to 62 +/- 4 beats min(-1), P < 0.05). Noradrenaline spillover and clearance were increased from pre-flight levels during baseline periods and during lower body suction, both in flight (n = 3) and on post-flight days 1 or 2 (n = 5, P < 0.05). In-flight baseline sympathetic nerve activity was increased above pre-flight levels (by 10-33 %) in the same three subjects in whom noradrenaline spillover and clearance were increased. The sympathetic response to 30 mmHg lower body suction was at pre-flight levels or higher in each subject (35 pre-flight vs. 40 bursts min(-1) in flight). No astronaut experienced presyncope during lower body suction in space (or during upright tilt following the Neurolab mission). We conclude that in space, baseline sympathetic neural outflow is increased moderately and sympathetic

  19. Chronic experimental myocardial infarction produces antinatriuresis by a renal nerve-dependent mechanism

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    Souza D.R.B.

    2004-01-01

    Full Text Available The present study focused on the role of sympathetic renal nerve activity, in mediating congestive heart failure-induced sodium retention following experimental chronic myocardial infarction. Groups of male Wistar rats (240-260 g were studied: sham-operated coronary ligation (CON3W, N = 11, coronary ligation and sham-operated renal denervation (INF3W, N = 19, 3 weeks of coronary ligation and sympathetic renal nerve denervation (INF3WDX, N = 6, sham-operated coronary ligation (N = 7, and 16 weeks of coronary ligation (INF16W, N = 7. An acute experimental protocol was used in which the volume overload (VO; 5% of body weight was applied for 30 min after the equilibration period of continuous iv infusion of saline. Compared to control levels, VO produced an increase (P < 0.01, ANOVA in urine flow rate (UFR; 570% and urinary sodium excretion (USE; 1117% in CON3W. VO induced a smaller increase (P < 0.01 in USE (684% in INF3W. A similar response was also observed in INF16W. In INF3WDX, VO produced an immediate and large increase (P < 0.01 in UFR (547% and USE (1211%. Similarly, in INF3W VO increased (P < 0.01 UFR (394% and USE (894%. Compared with INF3W, VO induced a higher (P < 0.01 USE in INF3WDX, whose values were similar to those for CON3W. These results suggest that renal sympathetic activity may be involved in sodium retention induced by congestive heart failure. This premise is supported by the observation that in bilaterally renal denervated INF3WDX rats myocardial infarction was unable to reduce volume expansion-induced natriuresis. However, the mechanism involved in urinary volume regulation seems to be insensitive to the factors that alter natriuresis.

  20. Differential cardiac responses to unilateral sympathetic nerve stimulation in the isolated innervated rabbit heart.

    Science.gov (United States)

    Winter, James; Tanko, Abdul Samed; Brack, Kieran E; Coote, John H; Ng, G André

    2012-01-26

    The heart receives both a left and right sympathetic innervation. Currently there is no description of an in vitro whole heart preparation for comparing the influence of each sympathetic supply on cardiac function. The aim was to establish the viability of using an in vitro model to investigate the effects of left and right sympathetic chain stimulation (LSS/RSS). For this purpose the upper sympathetic chain on each side was isolated and bipolar stimulating electrodes were attached between T2-T3 and electrically insulated from surrounding tissue in a Langendorff innervated rabbit heart preparation (n=8). Heart rate (HR) was investigated during sinus rhythm, whilst dromotropic, inotropic and ventricular electrophysiological effects were measured during constant pacing (250 bpm). All responses exhibited linear increases with increases in stimulation frequency (2-10 Hz). The change in HR was larger during RSS than LSS (P<0.01), increasing by 78±9 bpm and 49±8 bpm respectively (10 Hz, baseline; 145±7 bpm). Left ventricular pressure was increased from a baseline of 50±4 mmHg, by 22±5 mmHg (LSS, 10 Hz) and 4±1 mmHg (RSS, 10 Hz) respectively (P<0.001). LSS, but not RSS, caused a shortening of basal and apical monophasic action potential duration (MAPD90). We demonstrate that RSS exerts a greater effect at the sinoatrial node and LSS at the left ventricle. The study confirms previous experiments on dogs and cats, provides quantitative data on the comparative influence of right and left sympathetic nerves and demonstrates the feasibility of isolating and stimulating the ipsilateral cardiac sympathetic supply in an in vitro innervated rabbit heart preparation.

  1. Comparison of sympathetic nerve responses to neck and forearm isometric exercise

    Science.gov (United States)

    Steele, S. L. Jr; Ray, C. A.

    2000-01-01

    PURPOSE: Although the autonomic and cardiovascular responses to arm and leg exercise have been studied, the sympathetic adjustments to exercise of the neck have not. The purpose of the present study was twofold: 1) to determine sympathetic and cardiovascular responses to isometric contractions of the neck extensors and 2) to compare sympathetic and cardiovascular responses to isometric exercise of the neck and forearm. METHODS: Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate were measured in nine healthy subjects while performing isometric neck extension (INE) and isometric handgrip (IHG) in the prone position. After a 3-min baseline period, subjects performed three intensities of INE for 2.5 min each: 1) unloaded (supporting head alone), 2) 10% maximal voluntary contraction (MVC), and 3) 30% MVC, then subjects performed two intensities (10% and 30% MVC) of IHG for 2.5 min. RESULTS: Supporting the head by itself did not significantly change any of the variables. During [NE, MAP significantly increased by 10 +/- 2 and 31 +/- 4 mm Hg and MSNA increased by 67 +/- 46 and 168 +/- 36 units/30 s for 10% and 30% MVC, respectively. IHG and INE evoked similar responses at 10% MVC, but IHG elicited higher peak MAP and MSNA at 30% MVC (37 +/- 7 mm Hg (P architecture of the neck and forearm are responsible for these differences in peak responses.

  2. Comparison of sympathetic nerve responses to neck and forearm isometric exercise

    Science.gov (United States)

    Steele, S. L. Jr; Ray, C. A.

    2000-01-01

    PURPOSE: Although the autonomic and cardiovascular responses to arm and leg exercise have been studied, the sympathetic adjustments to exercise of the neck have not. The purpose of the present study was twofold: 1) to determine sympathetic and cardiovascular responses to isometric contractions of the neck extensors and 2) to compare sympathetic and cardiovascular responses to isometric exercise of the neck and forearm. METHODS: Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate were measured in nine healthy subjects while performing isometric neck extension (INE) and isometric handgrip (IHG) in the prone position. After a 3-min baseline period, subjects performed three intensities of INE for 2.5 min each: 1) unloaded (supporting head alone), 2) 10% maximal voluntary contraction (MVC), and 3) 30% MVC, then subjects performed two intensities (10% and 30% MVC) of IHG for 2.5 min. RESULTS: Supporting the head by itself did not significantly change any of the variables. During [NE, MAP significantly increased by 10 +/- 2 and 31 +/- 4 mm Hg and MSNA increased by 67 +/- 46 and 168 +/- 36 units/30 s for 10% and 30% MVC, respectively. IHG and INE evoked similar responses at 10% MVC, but IHG elicited higher peak MAP and MSNA at 30% MVC (37 +/- 7 mm Hg (P type composition, muscle mass, and/or muscle architecture of the neck and forearm are responsible for these differences in peak responses.

  3. Comparison of sympathetic nerve responses to neck and forearm isometric exercise

    Science.gov (United States)

    Steele, S. L. Jr; Ray, C. A.

    2000-01-01

    PURPOSE: Although the autonomic and cardiovascular responses to arm and leg exercise have been studied, the sympathetic adjustments to exercise of the neck have not. The purpose of the present study was twofold: 1) to determine sympathetic and cardiovascular responses to isometric contractions of the neck extensors and 2) to compare sympathetic and cardiovascular responses to isometric exercise of the neck and forearm. METHODS: Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate were measured in nine healthy subjects while performing isometric neck extension (INE) and isometric handgrip (IHG) in the prone position. After a 3-min baseline period, subjects performed three intensities of INE for 2.5 min each: 1) unloaded (supporting head alone), 2) 10% maximal voluntary contraction (MVC), and 3) 30% MVC, then subjects performed two intensities (10% and 30% MVC) of IHG for 2.5 min. RESULTS: Supporting the head by itself did not significantly change any of the variables. During [NE, MAP significantly increased by 10 +/- 2 and 31 +/- 4 mm Hg and MSNA increased by 67 +/- 46 and 168 +/- 36 units/30 s for 10% and 30% MVC, respectively. IHG and INE evoked similar responses at 10% MVC, but IHG elicited higher peak MAP and MSNA at 30% MVC (37 +/- 7 mm Hg (P muscle fiber type composition, muscle mass, and/or muscle architecture of the neck and forearm are responsible for these differences in peak responses.

  4. Effects of cervical sympathetic nerve stimulation on the cerebral microcirculation: possible clinical implications.

    Science.gov (United States)

    Passatore, M; Deriu, F; Roatta, S; Grassi, C; Micieli, G

    1996-01-01

    The action of bilateral cervical sympathetic nerve (CSN) stimulation on mean cerebral blood flow (CBF) and on its rhythmical fluctuations was studied in normotensive rabbits by using laser-Doppler flowmetry (LDF). A reduction in mean CBF, mediated by alpha-adrenoceptors, was the predominant effect; it was more often present and larger in size in the vascular beds supplied by the carotid than in those supplied by the vertebro-basilar system. This suggests that the sympathetic action facilitates a redistribution of blood flow to the brain stem. The effect induced by CSN stimulation on CBF spontaneous oscillations was a consistent decrease in amplitude and an increase in frequency, irrespective of the changes produced on the mean level of CBF. The possible implications of the sympathetic action on the state of the blood-brain barrier (BBB) are discussed. Experimental and clinical data dealing with the influence of sympathetic activation on the cerebrovascular system have been compared. As a result the possibility of analysing the spontaneous oscillations of CBF for clinical purposes is suggested.

  5. Effect of renal sympathetic denervation on atrial substrate remodeling in ambulatory canines with prolonged atrial pacing.

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    Xule Wang

    Full Text Available We have previously demonstrated that catheter-based renal sympathetic denervation (RSD could suppress atrial fibrillation (AF in canines with short-time rapid right atrial pacing (RAP. However, the role of renal denervation on atrial remodeling is unclear. The aim of the present study was to explore the long-term effect of RSD on the atrial remodeling during prolonged RAP. Twenty mongrel dogs were implanted with a high-frequency cardiac pacemaker with a transvenous lead inserted into the right atrial appendage. The dogs were divided into three groups: a sham-operated group (n = 6, the chronic RAP (CRAP group (n = 7, and the CRAP+RSD group (n = 7. In the CRAP+RSD group, a pacemaker was implanted 6 weeks after RSD was performed bilaterally for recovery. RAP was maintained for 5 weeks in CRAP group and CRAP+RSD group. The plasma levels of Angiotensin II and aldosterone were significantly increased in CRAP group compared with sham-operated group, but the increasing trend was inhibited in CRAP+RSD group compared with CRAP group (P<0.05. Similarly, RSD suppressed the increasing trend that prolonged RAP produced in the left atrial levels of ANP, TNF-α and IL-6. Compared with the sham-operated group, the CRAP group had significantly increased levels of caspase-3, bax and Cx40 whereas the level of Bcl-2 decreased (P<0.05. RSD markedly reduced the upregulation of caspase-3, bax and Cx40 and the downregulation of Bcl-2 expression compared with the CRAP group (P<0.05. Picric acid-sirius red staining study suggested that RSD could markedly alleviate the lesion degree of cardic fibrosis induced by CRAP (P<0.05. Immunohistochemistry results showed that the densities of TH- and GAP43- positive nerves were significantly elevated in the CRAP group compared with the sham-operated group, while RSD operation signicantly inhibited the these changes produced by CRAP. These findings suggest that renal denervation could suppress the atrial remodeling after

  6. Vestibular Modulation of Sympathetic Nerve Activity to Muscle and Skin in Humans

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    Elie Hammam

    2017-07-01

    Full Text Available We review the existence of vestibulosympathetic reflexes in humans. While several methods to activate the human vestibular apparatus have been used, galvanic vestibular stimulation (GVS is a means of selectively modulating vestibular afferent activity via electrodes over the mastoid processes, causing robust vestibular illusions of side-to-side movement. Sinusoidal GVS (sGVS causes partial entrainment of sympathetic outflow to muscle and skin. Modulation of muscle sympathetic nerve activity (MSNA from vestibular inputs competes with baroreceptor inputs, with stronger temporal coupling to the vestibular stimulus being observed at frequencies remote from the cardiac frequency; “super entrainment” was observed in some individuals. Low-frequency (<0.2 Hz sGVS revealed two peaks of modulation per cycle, with bilateral recordings of MSNA or skin sympathetic nerve activity, providing evidence of lateralization of sympathetic outflow during vestibular stimulation. However, it should be noted that GVS influences the firing of afferents from the entire vestibular apparatus, including the semicircular canals. To identify the specific source of vestibular input responsible for the generation of vestibulosympathetic reflexes, we used low-frequency (<0.2 Hz sinusoidal linear acceleration of seated or supine subjects to, respectively, target the utricular or saccular components of the otoliths. While others had discounted the semicircular canals, we showed that the contributions of the utricle and saccule to the vestibular modulation of MSNA are very similar. Moreover, that modulation of MSNA occurs at accelerations well below levels at which subjects are able to perceive any motion indicates that, like vestibulospinal control of posture, the vestibular system contributes to the control of blood pressure through potent reflexes in humans.

  7. Decreased adrenergic tone in acromegaly: evidence from direct recording of muscle sympathetic nerve activity.

    Science.gov (United States)

    Seravalle, G; Carzaniga, C; Attanasio, R; Grassi, G; Lonati, L; Facchini, C; Cozzi, R; Fatti, L M; Montini, M; Vitale, G; Sciortino, G; Damanti, S; Brambilla, G; Cavagnini, F; Mancia, G; Scacchi, M

    2012-08-01

    Sympathovagal imbalance has been shown in acromegaly by indirect measurements of adrenergic tone. Data regarding direct measurement of sympathetic activity are lacking as yet. Aim of this study was to assess the adrenergic tone through direct recording of muscle sympathetic nerve activity (MSNA) in acromegalic patients. Fifteen patients (age 26-66 years, eight women) with newly diagnosed active acromegaly without hyperprolactinaemia, pituitary hormone deficiencies, obstructive sleep apnoea and cardiac hypertrophy, and 15 healthy subjects matched for age, sex and body mass index were recruited. After evaluating anthropometric and echocardiographic parameters, anterior pituitary function, glucose and lipid metabolism, and measuring plasma leptin, direct recording of sympathetic outflow via the microneurographic technique was performed. For similar anthropometric and metabolic parameters in patients and controls, HOMA index was significantly increased in the former (4·2 ± 2·39 vs 1·6 ± 0·19, P < 0·001). Surprisingly, this finding of insulin resistance was accompanied by a marked sympathetic inhibition (MSNA 18·3 ± 8·10 vs 37·3 ± 6·48 bursts/min, P < 0·0001, respectively in patients and controls). A reduction in plasma leptin (1·6 ± 1·04 vs 6·5 ± 2·01 μg/l, P < 0·0001) was also recorded in the patients. MSNA was positively correlated with leptin (P < 0·0001). Newly diagnosed acromegalic patients without cardiac hypertrophy display a decreased sympathetic outflow in spite of insulin resistance. This finding might be related to hypoleptinaemia. © 2012 Blackwell Publishing Ltd.

  8. Sympathetic preganglionic efferent and afferent neurons mediated by the greater splanchnic nerve in rabbit

    Science.gov (United States)

    Torigoe, Yasuhiro; Cernucan, Roxana D.; Nishimoto, Jo Ann S.; Blanks, Robert H. I.

    1985-01-01

    As a part of the study of the vestibular-autonomic pathways involved in motion sickness, the location and the morphology of preganglionic sympathetic neurons (PSNs) projecting via the greater splanchnic nerve were examined. Retrograde labeling of neurons was obtained by application of horseradish peroxidase to the cut end of the greater splanchnic nerve. Labeled PSNs were found, ipsilaterally, within the T1 to T11 spinal cord segments, with the highest density of neurons in T6. Most PSNs were located within the intermediolateral column, but a significant portion also occurred within the lateral funiculus, the intercalated region, and the central autonomic area; the proportion of labeling between the four regions depended on the spinal cord segment.

  9. Nerve growth factor receptor from rabbit sympathetic ganglia membranes. Relationship between subforms.

    Science.gov (United States)

    Kouchalakos, R N; Bradshaw, R A

    1986-12-05

    The receptor for nerve growth factor (NGF) was purified from Triton X-100 extracts of sympathetic ganglia membranes by affinity chromatography on NGF-Sepharose. Elution of purified receptor was accomplished at pH 5 in the presence of 1 M NaCl. Sodium dodecyl sulfate gel electrophoresis of the purified iodinated receptor showed three major bands at Mr = 126,000, Mr = 105,000, and Mr = 81,000. Affinity labeling of the purified receptor using 125I-NGF and the photoreactive agent N-hydroxysuccinimidyl-p-azidobenzoate resulted in two major cross-linked complexes corresponding to Mr = 135,000 and Mr = 110,000. This labeling pattern is similar to that observed with sympathetic ganglia membranes (Massague, J., Guillette, B. J., Czech, M. P., Morgan, C. J., and Bradshaw, R. A. (1981) J. Biol. Chem. 256, 9419-9424) and indicates that these two forms do not arise from the cross-linking procedure. Reaction of the photoaffinity labeled NGF receptors with increasing amounts of trypsin resulted in a progressive decrease in the high molecular weight complex with a concomitant increase in the low molecular weight form. When the larger complex was isolated by electroelution from a sodium dodecyl sulfate gel and treated with trypsin, a species corresponding to Mr = 100,000 was generated. These observations are best explained by a precursor-product relationship for the two NGF receptor species of sympathetic neurons.

  10. Influence of ventilation and hypocapnia on sympathetic nerve responses to hypoxia in normal humans.

    Science.gov (United States)

    Somers, V K; Mark, A L; Zavala, D C; Abboud, F M

    1989-11-01

    The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.

  11. Less of insulin desensitization in sympathetic nerve terminals from wistar rats with insulin resistance.

    Science.gov (United States)

    Chi, T C; Liu, I M; Cheng, J T

    2000-04-12

    In an attempt to determine the effect of hyperinsulinemia on sympathetic function, release of norepinephrine (NE) from isolated aorta by insulin was measured in Wistar rats with insulin resistance. Insulin resistance was produced when the hypoglycemic action of glibenclamide at a dose of 10 mg/kg was almost abolished in rats that received daily injections of long-acting insulin for 15 days. Moreover, the stimulatory effect of insulin on glucose uptake was markedly reduced in both skeletal muscle strips and white adipocytes obtained from these rats with insulin resistance. However, the stimulatory effects of insulin at concentrations from 5 to 15 U/l on the release of NE from the aortic strip of insulin-resistant rats were not modified in the same manner but only slightly reduced compared with that of normal rats. These results suggest that insulin desensitization was produced later in sympathetic nerve terminals than in other organs in insulin-resistant rats and this may be helpful to explain the sympathetic hyperactivity associated with diabetes in clinics.

  12. Augmented supraorbital skin sympathetic nerve activity responses to symptom trigger events in rosacea patients.

    Science.gov (United States)

    Metzler-Wilson, Kristen; Toma, Kumika; Sammons, Dawn L; Mann, Sarah; Jurovcik, Andrew J; Demidova, Olga; Wilson, Thad E

    2015-09-01

    Facial flushing in rosacea is often induced by trigger events. However, trigger causation mechanisms are currently unclear. This study tested the central hypothesis that rosacea causes sympathetic and axon reflex-mediated alterations resulting in trigger-induced symptomatology. Twenty rosacea patients and age/sex-matched controls participated in one or a combination of symptom triggering stressors. In protocol 1, forehead skin sympathetic nerve activity (SSNA; supraorbital microneurography) was measured during sympathoexcitatory mental (2-min serial subtraction of novel numbers) and physical (2-min isometric handgrip) stress. In protocol 2, forehead skin blood flow (laser-Doppler flowmetry) and transepithelial water loss/sweat rate (capacitance hygrometry) were measured during sympathoexcitatory heat stress (whole body heating by perfusing 50°C water through a tube-lined suit). In protocol 3, cheek, forehead, forearm, and palm skin blood flow were measured during nonpainful local heating to induce axon reflex vasodilation. Heart rate (HR) and mean arterial pressure (MAP) were recorded via finger photoplethysmography to calculate cutaneous vascular conductance (CVC; flux·100/MAP). Higher patient transepithelial water loss was observed (rosacea 0.20 ± 0.02 vs. control 0.10 ± 0.01 mg·cm(-2)·min(-1), P rosacea and controls, respectively) stress was augmented in rosacea (both P rosacea compared with controls. No axon reflex vasodilation differences were observed between groups. These data indicate that rosacea affects SSNA and that hyperresponsiveness to trigger events appears to have a sympathetic component.

  13. Catheter based radiofrequency ablation of renal nerves for the treatment of resistant hypertension

    Directory of Open Access Journals (Sweden)

    Markus P. Schlaich

    2013-03-01

    Full Text Available Introduction Resistant hypertension is a common and growing clinical problem characterized by the failure to attain target blood pressure levels despite adequate use of at least three antihypertensive agents. Objectives The aim of this article is to emphasize the role of novel approaches to treat resistant hypertension. Materials and methods After an excursus on the physiological role of renal nerves on kidney function, volume homeostasis and blood pressure control, this article describes the radiofrequency ablation technology to obtain kidneys denervation. Results Activation of the sympathetic nervous system plays a prominent role as a major regulator of circulatory and metabolic control. The kidneys have a particularly dense afferent sensory and efferent sympathetic innervation and are thereby strategically positioned to be origin as well as target of sympathetic activation. In this context, recent evidence suggests that a novel catheter-based approach to functionally denervate the human kidneys using radiofrequency ablation technology may provide a safe and effective treatment alternative for resistant hypertension and its adverse consequences. Conclusions Despite the availability of numerous safe and effective pharmacological therapies to treat elevated blood pressure, novel therapeutic approaches are warranted to improve the management and prognosis of patients with refractory hypertension. Several clinical trials are currently conducted and planned to further substantiate the blood pressure lowering efficacy of this novel renal denervation procedure.

  14. [Expert consensus statement on interventional renal sympathetic denervation for hypertension treatment].

    Science.gov (United States)

    Mahfoud, F; Vonend, O; Bruck, H; Clasen, W; Eckert, S; Frye, B; Haller, H; Hausberg, M; Hoppe, U C; Hoyer, J; Hahn, K; Keller, T; Krämer, B K; Kreutz, R; Potthoff, S A; Reinecke, H; Schmieder, R; Schwenger, V; Kintscher, U; Böhm, M; Rump, L C

    2011-11-01

    This commentary summarizes the expert consensus and recommendations of the working group 'Herz und Niere' of the German Society of Cardiology (DGK), the German Society of Nephrology (DGfN) and the German Hypertension League (DHL) on renal denervation for antihypertensive treatment. Renal denervation is a new, interventional approach to selectively denervate renal afferent and efferent sympathetic fibers. Renal denervation has been demonstrated to reduce office systolic and diastolic blood pressure in patients with resistant hypertension, defined as systolic office blood pressure ≥ 160 mm Hg and ≥ 150 mm Hg in patients with diabetes type 2, which should currently be used as blood pressure thresholds for undergoing the procedure. Exclusion of secondary hypertension causes and optimized antihypertensive drug treatment is mandatory in every patient with resistant hypertension. In order to exclude pseudoresistance, 24-hour blood pressure measurements should be performed. Preserved renal function was an inclusion criterion in the Symplicity studies, therefore, renal denervation should be only considered in patients with a glomerular filtration rate > 45 ml/min. Adequate centre qualification in both, treatment of hypertension and interventional expertise are essential to ensure correct patient selection and procedural safety. Long-term follow-up after renal denervation and participation in the German Renal Denervation (GREAT) Registry are recommended to assess safety and efficacy after renal denervation over time.

  15. Renal artery sympathetic denervation: observations from the UK experience

    OpenAIRE

    Sharp, Andrew S. P.; Davies, Justin E.; Lobo, Melvin D.; Bent, Clare L.; Mark, Patrick B.; Burchell, Amy E; Thackray, Simon D.; Martin, Una; McKane, William S.; Gerber, Robert T.; Wilkinson, James R.; Antonios, Tarek F.; Doulton, Timothy W.; Patterson, Tiffany; Clifford, Piers C.

    2016-01-01

    Background Renal denervation (RDN) may lower blood pressure (BP); however, it is unclear whether medication changes may be confounding results. Furthermore, limited data exist on pattern of ambulatory blood pressure (ABP) response—particularly in those prescribed aldosterone antagonists at the time of RDN. Methods We examined all patients treated with RDN for treatment-resistant hypertension in 18 UK centres. Results Results from 253 patients treated with five technologies are shown. Pre-proc...

  16. Relationship of cardiac sympathetic nerve innervation and excitability to cardiac hypertrophy in very elderly male hypertensive patients.

    Science.gov (United States)

    Li, Shijun; Zhang, Li; Guo, Yuanyuan; Li, Xiaoying

    2013-09-01

    Our study aimed to disclose the relationship of cardiac sympathetic nerve innervation and excitability to myocardial hypertrophy in very old elderly male hypertensive patients with low serum testosterone level. A total of 80 elderly male hypertensive patients aged from 80 to 95 years were recruited. Heart rate variability is determined by 24 h dynamic electrocardiogram and heart rate variability analysis system. Cardiac function and left ventricular mass index were determined using color Doppler ultrasound. Standard deviation of all normal sinus R-R intervals over 24 h (SDNN) significantly decreased in hypertensive cardiac hypertrophy patients as compared with those without cardiac hypertrophy. SDANN and Standard deviation of the average normal sinus R-R intervals for all 5-min segment index, time-domain index reflecting sympathetic nerve tension, obviously decreased and LFnu and LFnu/HFnu, frequency-domain index representing sympathetic nerve excitability, significantly increased in hypertensive cardiac hypertrophy patients as compared with those without cardiac hypertrophy. Myocardial norepinephrine content significantly increased while tyrosine hydroxylase expression significantly lowered in hypertensive cardiac hypertrophy patients, and a negative correlation between myocardial tyrosine hydroxylase expression and myocardial norepinephrine content was present. Serum total testosterone level decreased in hypertensive cardiac hypertrophy patients and was an independent risk factor for the increase in myocardial norepinephrine content and decrease in tyrosine hydroxylase expression. These data confirm that cardiac sympathetic nerve hypoinnervation and relative increase in cardiac sympathetic nerve excitability are closely related to cardiac hypertrophy in very old hypertensive patients. A lower serum total testosterone level was the independent risk factor of cardiac sympathetic nerve hypoinnervation and relative increase in excitability in very old male

  17. A perspective on sympathetic renal denervation in chronic congestive heart failure.

    Science.gov (United States)

    Madanieh, Raef; El-Hunjul, Mohammed; Alkhawam, Hassan; Kosmas, Constantine E; Madanieh, Abed; Vittorio, Timothy J

    2016-01-01

    Medical therapy has indisputably been the mainstay of management for chronic congestive heart failure. However, a significant percentage of patients continue to experience worsening heart failure (HF) symptoms despite treatment with multiple therapeutic agents. Recently, catheter-based interventional strategies that interrupt the renal sympathetic nervous system have shown promising results in providing better symptom control in patients with HF. In this article, we will review the pathophysiology of HF for better understanding of the interplay between the cardiovascular system and the kidney. Subsequently, we will briefly discuss pivotal renal denervation (RDN) therapy trials in patients with resistant hypertension and then present the available evidence on the role of RDN in HF therapy.

  18. Muscle sympathetic nerve activity during cold stress and isometric exercise in healthy older adults.

    Science.gov (United States)

    Greaney, Jody L; Stanhewicz, Anna E; Kenney, W Larry; Alexander, Lacy M

    2014-09-15

    Cardiovascular mortality increases in cold weather in older adults, and physical activity may impart even greater cardiovascular risk than cold exposure alone. Human aging is associated with exaggerated pressor responses to whole body cooling; however, the sympathetic response to cold stress alone and in combination with isometric exercise is unknown. We hypothesized that cold stress would 1) increase muscle sympathetic nerve activity (MSNA) and 2) augment the MSNA response to isometric handgrip in older adults. Whole body cooling (water-perfused suit) was conducted in 11 young (23 ± 1 yr) and 12 healthy older adults (60 ± 2 yr). Blood pressure (BP; Finometer) and MSNA (microneurography) were measured throughout cooling and during isometric handgrip at 30% maximal voluntary contraction performed at a mean skin temperature (Tsk) of 34 and 30.5°C. MSNA was greater in older adults at Tsk = 34.0°C and throughout cooling (P 0.05) or older adults (Δ12 ± 1 Tsk 34°C vs. Δ8 ± 1 Tsk 30.5°C bursts/min; Δ18 ± 3 Tsk 34°C vs. Δ17 ± 2 Tsk 30.5°C mmHg; both P > 0.05). In summary, MSNA increased during cold stress in older, but not young, adults. Furthermore, concomitant cold stress did not alter the sympathetic responses to isometric exercise in either age group, suggesting preserved sympathetic responsiveness during exercise in the cold in healthy aging. Copyright © 2014 the American Physiological Society.

  19. Increased Efferent Cardiac Sympathetic Nerve Activity and Defective Intrinsic Heart Rate Regulation in Type 2 Diabetes.

    Science.gov (United States)

    Thaung, H P Aye; Baldi, J Chris; Wang, Heng-Yu; Hughes, Gillian; Cook, Rosalind F; Bussey, Carol T; Sheard, Phil W; Bahn, Andrew; Jones, Peter P; Schwenke, Daryl O; Lamberts, Regis R

    2015-08-01

    Elevated sympathetic nerve activity (SNA) coupled with dysregulated β-adrenoceptor (β-AR) signaling is postulated as a major driving force for cardiac dysfunction in patients with type 2 diabetes; however, cardiac SNA has never been assessed directly in diabetes. Our aim was to measure the sympathetic input to and the β-AR responsiveness of the heart in the type 2 diabetic heart. In vivo recording of SNA of the left efferent cardiac sympathetic branch of the stellate ganglion in Zucker diabetic fatty rats revealed an elevated resting cardiac SNA and doubled firing rate compared with nondiabetic rats. Ex vivo, in isolated denervated hearts, the intrinsic heart rate was markedly reduced. Contractile and relaxation responses to β-AR stimulation with dobutamine were compromised in externally paced diabetic hearts, but not in diabetic hearts allowed to regulate their own heart rate. Protein levels of left ventricular β1-AR and Gs (guanine nucleotide binding protein stimulatory) were reduced, whereas left ventricular and right atrial β2-AR and Gi (guanine nucleotide binding protein inhibitory regulatory) levels were increased. The elevated resting cardiac SNA in type 2 diabetes, combined with the reduced cardiac β-AR responsiveness, suggests that the maintenance of normal cardiovascular function requires elevated cardiac sympathetic input to compensate for changes in the intrinsic properties of the diabetic heart. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

  20. The effect of inflammation on sympathetic nerve mediated contractions in rat isolated caudal artery.

    Science.gov (United States)

    Fotso Soh, Jocelyn; Strong, Hilary R; Daneshtalab, Noriko; Tabrizchi, Reza

    2016-12-05

    Chronic inflammatory process(es) contributes to changes in vascular function in a variety of diseases. Sympathetic nerve-mediated responses in blood vessels play a pivotal role in regular physiological functions. We tested the hypothesis that sympathetic neuro-effector function will be altered as consequence of inflammatory state. Sympathetic nerve-mediated contractions and alpha adrenergic receptor expressions were evaluated in isolated caudal arteries of rats treated with saline and Complete Freund's adjuvant (CFA). While CFA-treated animals had significantly higher plasma levels of tumor necrosis factor-alpha compared to saline, blood pressure remained unchanged. Immunofluorescence revealed increased expression of ionized calcium adapter binding molecule-1 in the adventitia of blood vessels from CFA-treated animals compared to saline. In isolated arteries, electrical field stimulations between 1.25 and 40Hz resulted in frequency-dependent contractions that wasabolished by tetrodotoxin. Neurogenic contractions from CFA groups were significantly greater than saline. While the presence of alpha1-adrenoceptor antagonist (prazosin) significantly inhibited contractions at lower frequencies of stimulation (1.25-5Hz) in isolated arteries of CFA-treated rats compared to controls, alpha2-adrenoceptor antagonist (rauwolscine) had modest effects. Inhibition of neuronal reuptake by cocaine comparably enhanced field-stimulated responses in vessels of experimental and control animals. Immunofluorescence revealed a difference in expression of alpha1- and alpha2-adrenoceptors in the endothelium of blood vessels of CFA compared to saline controls. Collectively, our observations lend support to enhanced neurogenic contractions in blood vessels of inflamed animals possibly attributing to alterations in responsiveness and/or distribution of post-junctional alpha1-adrenoceptors.

  1. Changes in heart rate, blood pressure and renal sympathetic nerve activity induced by microinjection of capsaicin into area postrema in rats%最后区微量注射辣椒素对大鼠血压、心率和肾交感神经放电的影响

    Institute of Scientific and Technical Information of China (English)

    薛保建; 何瑞荣

    2000-01-01

    The effects of capsaicin microinjection into area postrema (AP) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in 36 anesthetized Sprague-Dawley rats. The results obtained are as follows. (1) Following microinjection of capsaicin (10 μmol/L, 50 nl) into the AP, MAP, HR and RSNA were significantly increased from 12.34±0.53 kPa, 328.52±7.54 bpm and 100±0% to 15.17±0.25 kPa (P<0.001), 354.81±8.54 bpm (P<0.001) and 156.95±7.57% (P<0.001), respectively. (2) Ruthenium red (RR, 100 mmol/L, 0.2 ml, iv), a capsaicin receptor antagonist, significantly inhibited these effects of capsaicin. (3) Pretreatment with a NMDA receptor antagonist MK-801 (500 μg/kg, 0.2 ml, iv) also reduced these effects of capsaicin. The above results indicate that microinjection of capsaicin into AP induces excitatory effects on MAP, HR and RSNA, which are mediated by capsaicin receptors with glutamate involvement.%在36只麻醉Sprague-Dawley大鼠, 观察了最后区内微量注射辣椒素(10 μmol/L, 50 nl)对平均动脉压(MAP)、心率(HR)和肾交感神经放电(RSNA)的影响.实验结果如下:(1)最后区内注射辣椒素可引起 MAP、HR 和RSNA明显增加, 分别由12.34±0.53 kPa、 328.52±7.54 bpm 和100±0% 增至15.17±0.25 kPa (P<0.001)、 354.81±8.54 bpm (P<0.001) 和156.95±7.57% (P<0.001);(2) 静脉注射辣椒素受体阻断剂钌红(100 mmol/L, 0.2 ml) 后, 辣椒素的上述效应可被明显抑制;(3) 预先应用NMDA 受体阻断剂MK-801 (500 μg/kg, 0.2 ml, iv)也明显抑制辣椒素的兴奋效应.以上结果提示, 最后区微量注射辣椒素对血压、心率和肾交感神经放电有兴奋作用, 而此作用由辣椒素受体介导并有谷氨酸参与.

  2. Effect of pioglitazone on muscle sympathetic nerve activity in type 2 diabetes mellitus with α-glucosidase inhibitor.

    Science.gov (United States)

    Kobayashi, Daisuke; Takamura, Masayuki; Murai, Hisayoshi; Usui, Soichiro; Ikeda, Tatsunori; Inomata, Jun-ichiro; Takashima, Shin-ichiro; Kato, Takeshi; Furusho, Hiroshi; Takeshita, Yumie; Ota, Tsuguhito; Takamura, Toshinari; Kaneko, Shuichi

    2010-12-08

    Activation of the sympathetic nervous system is augmented in patients with type 2 diabetes mellitus (DM). Pioglitazone, an anti-diabetic drug, improves insulin resistance, but its influence on sympathetic nerve activity is not clear. To identify the relationship between insulin resistance and sympathetic activity, we examined muscle sympathetic nerve activity (MSNA) in controlled type 2 DM patients with alpha-glucosidase inhibitor (GI). We measured MSNA and calculated homeostasis model assessment of insulin resistance index (HOMA-IR) in twelve DM patients treated with alpha-GI and thirteen age-matched healthy subjects. In DM patients with alpha-GI, all parameters were reexamined after three months of treatment with pioglitazone. MSNA and HOMA-IR were significantly greater in DM patients with alpha-GI compared to healthy subjects. Hemoglobin A1c did not differ in DM patients before and after pioglitazone. However, pioglitazone significantly decreased MSNA in DM patients compared with alpha-GI (21.7±5.2 vs. 32.0±6.8 burst/min, ppioglitazone was similar to that in healthy subjects. HOMA-IR significantly decreased after pioglitazone, and a significant relationship was found between the absolute change in MSNA and HOMA-IR (r=0.65, ppioglitazone provides an additional effect on inhibition of sympathetic nerve activity.

  3. The role of NGF in pregnancy-induced degeneration and regeneration of sympathetic nerves in the guinea pig uterus.

    Science.gov (United States)

    Brauer, M M; Shockley, K P; Chávez, R; Richeri, A; Cowen, T; Crutcher, K A

    2000-02-14

    In the guinea pig, pregnancy is associated with a generalised depletion of noradrenaline in uterine sympathetic nerves and, in the areas of the uterus surrounding the foetus, by a complete degeneration of sympathetic nerve fibres. These pregnancy-induced changes have been interpreted as a selective effect of placental hormones on the system of short sympathetic fibres arising from the paracervical ganglia. An alternative explanation is that pregnancy affects the neurotrophic capacity of the uterus. We measured NGF-protein levels in the guinea pig uterine horn, tubal end and cervix at early pregnancy, late pregnancy and early postpartum, using a two-site enzyme-linked immunosorbent assay. For comparative purposes the distribution and relative density of noradrenaline-containing sympathetic nerve fibres were assessed histochemically, and tissue levels of noradrenaline were measured biochemically, using high-performance liquid chromatography with electrochemical detection. In all the uterine regions analysed, NGF-protein levels showed a decline at term pregnancy, but in no case was this change statistically significant. After delivery, NGF-protein levels showed a marked increase in the cervix as well as in both the fertile and empty horns. These results suggest that alterations in NGF-protein do not account for the impairment of uterine sympathetic innervation during pregnancy, but may contribute to their recovery after delivery.

  4. Sympathetic nerve fibers sprout into rat odontoblast layer, but not into dentinal tubules, in response to cavity preparation.

    Science.gov (United States)

    Shimeno, Yoichi; Sugawara, Yumiko; Iikubo, Masahiro; Shoji, Noriaki; Sasano, Takashi

    2008-04-11

    This study was designed to determine if sympathetic nerve fibers exist in dentinal tubules in rat normal dental pulp, and if they sprout into the dentinal tubules in response to artificial cavity preparation in dentin. Sympathetic nerve fibers in rat molar dental pulp were labeled using an anterograde axonal transport technique involving injection of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the superior cervical ganglion (SCG). They were then observed using light and electron microscopes. In normal dental pulp (control), scattered WGA-HRP reaction products were observed in unmyelinated nerve endings in the odontoblast layer and subodontoblastic region. In injured pulp 3 weeks after cavity preparation, reaction products were about 1.8-times more plentiful in the above areas (versus control pulp). However, no labeled nerve fibers were observed in the dentinal tubules in either control or injured dental pulp. These results indicate that although sympathetic nerve fibers do indeed sprout in rat dental pulp in response to cavity preparation, they do not penetrate into the dentinal tubules in which postganglionic nerve endings derived from the SCG were not originally present.

  5. Sympathetic activity is increased in polycystic kidney disease and is associated with hypertension

    NARCIS (Netherlands)

    Klein, IHHT; Ligtenberg, G; Oey, PL; Koomans, HA; Blankestijn, PJ

    2001-01-01

    Hypertension is common in patients with polycystic kidney disease (PKD). This study addresses the hypothesis that sympathetic activity is enhanced in hypertensive PKD patients, not only when renal function is impaired but also when renal function is still normal. Muscle sympathetic nerve activity (M

  6. Non-invasive vagus nerve stimulation in healthy humans reduces sympathetic nerve activity.

    OpenAIRE

    Clancy, JA; Mary, DA; Witte, KK; Greenwood, JP; Deuchars, SA; Deuchars, J

    2014-01-01

    Background: Vagus nerve stimulation (VNS) is currently used to treat refractory epilepsy and is being investigated as a potential therapy for a range of conditions, including heart failure, tinnitus, obesity and Alzheimer's disease. However, the invasive nature and expense limits the use of VNS in patient populations and hinders the exploration of the mechanisms involved. Objective: We investigated a non-invasive method of VNS through electrical stimulation of the auricular branch of the vagu...

  7. Sympathetic nerve activity can be estimated from skin conductance responses - a comment on Henderson et al. (2012).

    Science.gov (United States)

    Bach, Dominik R

    2014-01-01

    A recent paper by Henderson et al. (2012) claimed that skin sympathetic nerve activity (SSNA) can not be retrieved from skin conductance responses (SCR). Here, I argue that this claim is not supported by the literature, and comment on contemporary approaches of estimating SSNA from SCR using biophysical models. © 2013.

  8. A vesicular sequestration to oxidative deamination shift in myocardial sympathetic nerves in Parkinson's disease.

    Science.gov (United States)

    Goldstein, David S; Sullivan, Patricia; Holmes, Courtney; Miller, Gary W; Sharabi, Yehonatan; Kopin, Irwin J

    2014-10-01

    In Parkinson's disease (PD), profound putamen dopamine (DA) depletion reflects denervation and a shift from vesicular sequestration to oxidative deamination of cytoplasmic DA in residual terminals. PD also involves cardiac sympathetic denervation. Whether PD entails myocardial norepinephrine (NE) depletion and a sequestration-deamination shift have been unknown. We measured apical myocardial tissue concentrations of NE, DA, and their neuronal metabolites 3,4-dihydroxyphenylglycol (DHPG), and 3,4-dihydroxyphenylacetic acid (DOPAC) from 23 PD patients and 23 controls and ascertained the extent of myocardial NE depletion in PD. We devised, validated in VMAT2-Lo mice, and applied 5 neurochemical indices of the sequestration-deamination shift-concentration ratios of DOPAC:DA, DA:NE, DHPG:NE, DOPAC:NE, and DHPG:DOPAC-and used a kinetic model to estimate the extent of the vesicular storage defect. The PD group had decreased myocardial NE content (p Parkinson's disease (PD) patients have profound (98%) myocardial norepinephrine depletion, because of both cardiac sympathetic denervation and a shift from vesicular sequestration to oxidative deamination of cytoplasmic catecholamines in the residual nerves. This shift may be part of a final common pathogenetic pathway in the loss of catecholaminergic neurons that characterizes PD.

  9. Muscle sympathetic nerve activity and volume regulating factors in healthy pregnant and non-pregnant women.

    Science.gov (United States)

    Charkoudian, Nisha; Usselman, Charlotte W; Skow, Rachel J; Staab, Jeffery S; Julian, Colleen Glyde; Stickland, Michael K; Chari, Radha S; Khurana, Rshmi; Davidge, Sandra T; Davenport, Margie H; Steinback, Craig D

    2017-07-21

    Healthy, normotensive human pregnancies are associated with striking increases in both plasma volume and vascular sympathetic nerve activity (SNA). In non-pregnant humans, volume regulatory factors including plasma osmolality, vasopressin and the renin-angiotensin-aldosterone system have important modulatory effects on control of sympathetic outflow. We hypothesized that pregnancy would be associated with changes in the relationships between SNA (measured as muscle SNA) and volume regulating factors, including plasma osmolality, plasma renin activity and arginine vasopressin (AVP). We studied 46 healthy, normotensive young women (23 pregnant and 23 non-pregnant). We measured SNA, arterial pressure, plasma osmolality, plasma renin activity, AVP and other volume regulatory factors in resting, semi-recumbent posture. Pregnant women had significantly higher resting SNA (38 ± 12 vs. non-pregnant: 23 ± 6 bursts/minute), lower osmolality and higher plasma renin activity and aldosterone (all P pregnant] vs. 5.17 ± 2.03 [pregnant], P > 0.05). However, regression analysis detected a significant relationship between individual values for SNA and AVP in pregnant (r = 0.71, P pregnant women (r = 0.04). No relationships were found for other variables. These data suggest that the link between AVP release and resting SNA becomes stronger in pregnancy, which may contribute importantly to blood pressure regulation in healthy women during pregnancy. Copyright © 2017, American Journal of Physiology-Heart and Circulatory Physiology.

  10. Role of sympathetic nerves in the establishment of metastatic breast cancer cells in bone

    Directory of Open Access Journals (Sweden)

    Florent Elefteriou

    2016-09-01

    Full Text Available The bone marrow microenvironment is characterized by its multicellular nature, and perhaps less obviously by the high mobility of multiple transient and stationary cell lineages present in this environment. The trafficking of hematopoietic and mesenchymal cells between the bone marrow and blood compartments is regulated by a number of bone marrow-derived factors. It is suspected that transformed metastatic cells “hijack” these processes to engraft into the skeleton and eventually cause the skeletal complications associated with metastatic disease. In this short review, experimental and association data supporting the contribution of a less recognized cell type of the bone marrow – the nerves of the sympathetic nervous system – to early events of the breast cancer bone metastatic process, are summarized.

  11. WE-E-BRE-02: BEST IN PHYSICS (THERAPY) - Stereotactic Radiotherapy for Renal Sympathetic Ablation for the Treatment of Refractory Hypertension

    Energy Technology Data Exchange (ETDEWEB)

    Maxim, P; Wheeler, M; Loo, B [Stanford University, Stanford, CA (United States); Maguire, P [Cyberheart, Inc., Sunnyvale, CA (United States)

    2014-06-15

    Purpose: To determine the safety and efficacy of stereotactic radiotherapy as a novel treatment for patients with refractory hypertension in a swine model. Uncontrolled hypertension is a significant contributor to morbidity and mortality, substantially increasing the risk of ischemic stroke, ischemic heart disease, and kidney failure. Methods: High-resolution computed tomography (CT) images of anesthetized pigs were acquired and treatment plans for each renal artery and nerve were developed using our clinically implemented treatment planning system. Stereotactic radiotherapy, 40Gy in single fraction was delivered bilaterally to the renal nerves using a state-of-the-art medical linear accelerator under image guidance utilizing dynamic conformal arcs. Dose to nearby critical organs was evaluated by dosevolume histogram analysis and correlated to toxicity data obtained through follow up pathology analysis. The animals were observed for six months with serial measurements of blood pressure, urine analysis, serum laboratories, and overall clinical and behavioral status. Results: All animals survived to the follow-up point without evidence of renal dysfunction (stable serum creatinine), skin changes, or behavioral changes that might suggest animal discomfort. Plasma norepinephrine levels (ng/ml) were followed monthly for 6 months. The average reduction observed was 63%, with the median reduction at 73.5%. Microscopic evaluation 4–6 weeks after treatment showed evidence of damage to the nerves around treated renal arteries. Considerable attenuation in pan neurofilament expression by immunohistochemistry was observed with some vacuolar changes indicative of injury. There was no histological or immunohistochemical evidence of damage to nearby spinal cord or spinal nerve root structures. Conclusion: Our preclinical studies have shown stereotactic radiotherapy to the renal sympathetic plexus to be safe and effective in reducing blood pressure, thus this approach holds great

  12. A Case Report of Renal Sympathetic Denervation for the Treatment of Polymorphic Ventricular Premature Complexes

    Science.gov (United States)

    Kiuchi, Márcio Galindo; Vitorio, Frederico Puppim; da Silva, Gustavo Ramalho; Paz, Luis Marcelo Rodrigues; Souto, Gladyston Luiz Lima

    2015-01-01

    Abstract Premature ventricular complexes are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Recently, Armaganijan et al reported the relevance of sympathetic activation in patients with ventricular arrhythmias and suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden. In this report, we describe a 32-year-old hypertensive male patient presenting with a high incidence of polymorphic premature ventricular complexes on a 24 hour Holter monitor. Beginning 1 year prior, the patient experienced episodes of presyncope, syncope, and tachycardia palpitations. The patient was taking losartan 100 mg/day, which kept his blood pressure (BP) under control, and sotalol 160 mg twice daily. Bisoprolol 10 mg/day was used previously but was not successful for controlling the episodes. The 24 hour Holter performed after the onset of sotalol 160 mg twice daily showed a heart rate ranging between 48 (minimum)–78 (average)–119 (maximum) bpm; 14,286 polymorphic premature ventricular complexes; 3 episodes of nonsustained ventricular tachycardia, the largest composed of 4 beats at a rate of 197 bpm; and 14 isolated atrial ectopic beats. Cardiac magnetic resonance imaging with gadolinium perfusion performed at rest and under pharmacological stress with dipyridamole showed increased left atrial internal volume, preserved systolic global biventricular function, and an absence of infarcted or ischemic areas. The patient underwent bilateral renal sympathetic denervation. The only drug used postprocedure was losartan 25 mg/day. Three months after the patient underwent renal sympathetic denervation, the mean BP value dropped to 132/86 mmHg, the mean systolic/diastolic 24 hour ambulatory BP measurement was reduced to 128/83

  13. The sympathetic nervous system alterations in human hypertension.

    Science.gov (United States)

    Grassi, Guido; Mark, Allyn; Esler, Murray

    2015-03-13

    Several articles have dealt with the importance and mechanisms of the sympathetic nervous system alterations in experimental animal models of hypertension. This review addresses the role of the sympathetic nervous system in the pathophysiology and therapy of human hypertension. We first discuss the strengths and limitations of various techniques for assessing the sympathetic nervous system in humans, with a focus on heart rate, plasma norepinephrine, microneurographic recording of sympathetic nerve traffic, and measurements of radiolabeled norepinephrine spillover. We then examine the evidence supporting the importance of neuroadrenergic factors as promoters and amplifiers of human hypertension. We expand on the role of the sympathetic nervous system in 2 increasingly common forms of secondary hypertension, namely hypertension associated with obesity and with renal disease. With this background, we examine interventions of sympathetic deactivation as a mode of antihypertensive treatment. Particular emphasis is given to the background and results of recent therapeutic approaches based on carotid baroreceptor stimulation and radiofrequency ablation of the renal nerves.

  14. Revisiting renovascular imaging for renal sympathetic denervation: current techniques and applications

    Energy Technology Data Exchange (ETDEWEB)

    Pua, Uei; Tan, Cher Heng [Tan Tock Seng Hospital, Department of Diagnostic Radiology, Singapore (Singapore); Ho, Hee Hwa; Tan, Julian Ko Beng; Ong, Paul Jau Leong [Tan Tock Seng Hospital, Department of Cardiology, Singapore (Singapore)

    2014-08-28

    Renal sympathetic denervation (RDN) is an emerging technique in the treatment of resistant hypertension, most commonly performed using an endovascular approach. Clinical and anatomical criteria for RDN are well established and imaging plays an integral role in selecting patients with suitable anatomy, procedural planning and device selection. Nevertheless, the current body of literature surrounding imaging related to RDN remains limited. The purpose of this article is to illustrate the expectations and limitations of various imaging techniques, including Doppler ultrasound, CT angiography, MR angiography and newer techniques such as non-contrast MR angiography, in the context of RDN. (orig.)

  15. The brain subfornical organ mediates leptin-induced increases in renal sympathetic activity but not its metabolic effects.

    Science.gov (United States)

    Young, Colin N; Morgan, Donald A; Butler, Scott D; Mark, Allyn L; Davisson, Robin L

    2013-03-01

    The adipocyte-derived hormone leptin acts within the central nervous system to decrease food intake and body weight and to increase renal and thermogenic brown adipose tissue sympathetic nerve activity (SNA). Previous studies have focused on hypothalamic brain regions, although recent findings have identified leptin receptors (ObR) in a distributed brain network, including the circumventricular subfornical organ (SFO), a forebrain region devoid of a blood-brain barrier. We tested the hypothesis that ObR in the SFO are functionally linked to leptin-induced decreases in food intake and body weight and increases in SNA. SFO-targeted microinjections of an adenovirus encoding Cre-recombinase in ObR(flox/flox) mice resulted in selective ablation of ObR in the SFO. Interestingly, deletion of ObR in the SFO did not influence the decreases in either food intake or body weight in response to daily systemic or cerebroventricular administration of leptin. In line with these findings, reduction in SFO ObR did not attenuate leptin-mediated increases in thermogenic brown adipose tissue SNA. In contrast, increases in renal SNA induced by systemic or cerebroventricular administration of leptin were abolished in mice with SFO-targeted deletion of ObR. These results demonstrate that ObR in the SFO play an important role in leptin-induced renal sympathoexcitation, but not in the body weight, food intake, or brown adipose tissue SNA thermogenic effects of leptin. These findings highlight the concept of a distributed brain network of leptin action and illustrate that brain regions, including the SFO, can mediate distinct cardiovascular and metabolic responses to leptin.

  16. Autonomic markers of emotional processing: skin sympathetic nerve activity in humans during exposure to emotionally-charged images

    Directory of Open Access Journals (Sweden)

    Rachael eBrown

    2012-10-01

    Full Text Available The sympathetic innervation of the skin primarily subserves thermoregulation, but the system has also been commandeered as a means of expressing emotion. While it is known that the level of skin sympathetic nerve activity (SSNA is affected by anxiety, the majority of emotional studies have utilized the galvanic skin response as a means of inferring increases in SSNA. The purpose of the present study was to characterize the changes in SSNA when showing subjects neutral or emotionally-charged images from the International Affective Picture System. Skin sympathetic nerve activity was recorded via tungsten microelectrodes inserted into cutaneous fascicles of the common peroneal nerve in ten subjects. Neutral images, positively-charged images (erotica or negatively-charged images (mutilation were presented in blocks of fifteen images of a specific type, each block lasting two minutes. Images of erotica or mutilation were presented in a quasi-random fashion, each block following a block of neutral images. Both images of erotica or images of mutilation caused significant increases in SSNA, but the increases in SSNA were greater for mutilation. The increases in SSNA were often coupled with sweat release and cutaneous vasoconstriction, however, these markers were not always consistent with the SSNA increases. We conclude that SSNA, comprising cutaneous vasoconstrictor and sudomotor activity, increases with both positively-charged and negatively-charged emotional images. Measurement of SSNA provides a more comprehensive assessment of sympathetic outflow to the skin than does the use of sweat release alone as a marker of emotional processing.

  17. Effect of contraction intensity on sympathetic nerve activity to active human skeletal muscle

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    Daniel eBoulton

    2014-06-01

    Full Text Available The effect of contraction intensity on muscle sympathetic nerve activity (MSNA to active human limbs has not been established. To address this, MSNA was recorded from the left peroneal nerve during and after dorsiflexion contractions sustained for two minutes by the left leg at ~10, 25 and 40 %MVC. To explore the involvement of the muscle metaboreflex, limb ischaemia was imposed midway during three additional contractions and maintained during recovery. Compared with total MSNA at rest (11.5 ± 4.1 mv.min-1, MSNA in the active leg increased significantly at the low (21.9 ± 13.6 mv.min-1, medium (30.5 ± 20.8 mv.min-1 and high (50.0 ± 24.5 mv.min-1 intensities. This intensity-dependent effect was more strongly associated with increases in MSNA burst amplitude than burst frequency. Total MSNA then returned to resting levels within the first minute of recovery. Limb ischaemia had no significant influence on the intensity-dependent rise in MSNA or its decline during recovery in the active leg. These findings reveal intensity-dependent increases in total MSNA and burst amplitude to contracting human skeletal muscle that do not appear to involve the muscle metaboreflex.

  18. Contributions of central command and muscle feedback to sympathetic nerve activity in contracting human skeletal muscle

    Directory of Open Access Journals (Sweden)

    Daniel eBoulton

    2016-05-01

    Full Text Available During voluntary contractions, muscle sympathetic nerve activity (MSNA to contracting muscles increases in proportion to force but the underlying mechanisms are not clear. To shed light on these mechanisms, particularly the influences of central command and muscle afferent feedback, the present study tested the hypothesis that MSNA is greater during voluntary compared with electrically-evoked contractions. Seven male subjects performed a series of 1-minute isometric dorsiflexion contractions (left leg separated by 2-minute rest periods, alternating between voluntary and electrically-evoked contractions at similar forces (5-10 % of maximum. MSNA was recorded continuously (microneurography from the left peroneal nerve and quantified from cardiac-synchronised, negative-going spikes in the neurogram. Compared with pre-contraction values, MSNA increased by 51 ± 34 % (P 0.05. MSNA analysed at 15-s intervals revealed that this effect of voluntary contraction appeared 15-30 s after contraction onset (P < 0.01, remained elevated until the end of contraction, and disappeared within 15 s after contraction. These findings suggest that central command, and not feedback from contracting muscle, is the primary mechanism responsible for the increase in MSNA to contracting muscle. The time-course of MSNA suggests that there is a longer delay in the onset of this effect compared with its cessation after contraction.

  19. Acupuncture Attenuates Renal Sympathetic Activity and Blood Pressure via Beta-Adrenergic Receptors in Spontaneously Hypertensive Rats

    Science.gov (United States)

    Ye, Yang; Wang, Xue-Rui; Li, Fang; Xiao, Ling-Yong; Shi, Guang-Xia

    2017-01-01

    The sympathetic nervous system, via epinephrine and norepinephrine, regulates β-adrenergic receptor (β-AR) expression, and renal sympathetic activation causes sustained increases in blood pressure by enhanced renin release. In this study, we aim to investigate the effect and underlying mechanism of acupuncture at Taichong (LR3) on renal sympathetic activity in spontaneously hypertensive rats. Unanesthetized rats were subject to daily acupuncture for 2 weeks. Mean blood pressure (MBP) and heart rate variability (HRV) were monitored at days 0, 7, and 14 by radiotelemetry. After euthanasia on the 14th day, blood and the kidneys were collected and subject to the following analyses. Epinephrine and norepinephrine were detected by ELISA. The expression of β-ARs was studied by western blotting and PCR. The renin content was analyzed by radioimmunoassay. 14-day acupuncture significantly attenuates the increase of MBP. The HRV indices, the standard deviation of all normal NN intervals (SDNN), and the ratio of the low-frequency component to the high-frequency component (LF/HF) were improved following acupuncture. Renal sympathetic activation induced upregulation of epinephrine, norepinephrine, and renin content were attenuated by acupuncture. In addition, acupuncture decreased β1-AR expression and improved β2-AR expression. These results indicated that acupuncture relieves the increased MBP via the regulation of renal sympathetic activity and β-ARs. PMID:28270938

  20. Increased sympathetic nerve activity correlates with neurovascular compression at the rostral ventrolateral medulla.

    Science.gov (United States)

    Sendeski, Mauricio M; Consolim-Colombo, Fernanda Marciano; Leite, Claudia Costa; Rubira, Marcelo Custódio; Lessa, Patricia; Krieger, Eduardo Moacyr

    2006-05-01

    We used microneurography to measure muscle sympathetic nerve activity (MSNA) in 25 hypertensive subjects and correlated these results with the presence or absence of signs of neurovascular compression (NVC) at the rostral ventrolateral (RVL) medulla on MRI. Subjects were divided into 3 groups based on MRI findings: NVC-, no MRI evidence of NVC (N=9); NVC+contact, image showing artery in contact but not compressing the RVL medulla (N=8); and NVC+compression, image showing arterial compression of the RVL medulla (N=8). The MSNA measurements were performed at rest, after a hypothermic stimulus, and during isometric exercise. The MSNA during rest in the NVC+compression group was significantly higher than that in the NVC+contact and NVC- groups (30.4+/-3.4 versus 17.5+/-1.1 and 21.4+/-3.2 spikes per minute, respectively). However, the blood pressure in the NVC+compression group was slightly but not significantly higher than that in the other 2 groups (183+/-7/115+/-8, 174+/-6/108+/-7, and 171+/-5/110+/-5 mm Hg, respectively). The increases in MSNA, blood pressure, and heart rate during the cold pressor and isometric exercise tests were similar. Our results show that, although resting MSNA is elevated in patients with true NVC of the RVL medulla, patients without NVC or with arterial contact but not overt compression of the RVL medulla have similar MSNA. These findings are important for identifying, among hypertensive patients with NVC, individuals who may have associated physiological repercussions, such as increased sympathetic activity.

  1. Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans

    Directory of Open Access Journals (Sweden)

    Masashi eIchinose

    2012-08-01

    Full Text Available The mechanisms by which blood pressure is maintained against the orthostatic stress caused by gravity’s effect on the fluid distribution within the body are important issues in physiology, especially in humans who usually adopt an upright posture. Peripheral vasoconstriction and increased heart rate are major cardiovascular adjustments to orthostatic stress and comprise part of the reflex response elicited via the carotid sinus and aortic baroreceptors (arterial baroreflex: ABR and cardiopulmonary stretch receptors (cardiopulmonary baroreflex. In a series of studies, we have been characterizing the ABR-mediated regulation of cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA while applying orthostatic stress in humans. We have found that under orthostatic stress, dynamic carotid baroreflex responses are modulated as exemplified by the increases in the MSNA, blood pressure and heart rate responses elicited by carotid baroreflex unloading and the shorter period of MSNA suppression, comparable reduction and faster recovery of MAP and greater heart rate response to carotid baroreflex stimulation. Our results also show that ABR-mediated beat-to-beat control over burst incidence, burst strength and total MSNA is progressively modulated as orthostatic stress is increased until induction of syncope, and that the sensitivity of ABR control over the aforementioned MSNA variables is substantially reduced during the development of syncope. We suggest that in humans, the modulation of ABR function under orthostatic stress may be one of the mechanisms by which blood pressure is maintained and orthostatic hypotension limited, and impairment of ABR control over sympathetic vasomotor activity leads to the severe hypotension associated with orthostatic syncope.

  2. Renal sympathetic nerve activity associated with the severity of heart failure in dogs with chronic heart failure%慢性心力衰竭犬肾交感神经活性与心衰严重程度的关系

    Institute of Scientific and Technical Information of China (English)

    陈平安; 罗仪山; 阳军; 李韶南; 雷晓明

    2015-01-01

    Objective To investigate the relationship between renal sympathetic nerve activity and the severity of heart failure in dogs with chronic heart failure ( CHF) .Methods CHF were induced by ab-dominal aorta constriction.Plasma renin activity ( PRA) , adrenaline ( E) , and noradrenaline ( NE) were determined in 9 dogs with CHF (CHF group) and 3 sham-operated dogs (control group).Results E, NE, PRA, and B-type natriuretic peptide ( BNP) were significantly higher in CHF group than those in con-trol group (all P <0.01).Compared to 10-week post-operation, PRA [(2.08 ±0.08)ng/(ml・ h) vs (2.26 ±0.16)ng/(ml・ h)], NE [(184.01 ±11.76)pg/ml vs (202.99 ±16.54)pg/ml] and BNP [(85.87 ±11.41)μg/ml vs (100.41 ±9.24)μg/ml] were significantly increased in the 12-week post-op-eration (all P <0.01).PRA [10 weeks post-operation:(2.13 ±0.08)ng/(ml・ h) vs (2.02 ±0.05)ng/(ml・ h);12 weeks post-operation:(2.38 ±0.09)ng/(ml・ h) vs (2.11 ±0.07)ng/(ml・ h)] and NE [10 weeks post-operation: (191.75 ±8.40) pg/ml vs (174.33 ±7.08) pg/ml;12 weeks post-operation:(215.69 ±6.26)pg/ml vs (186.36 ±7.98)pg/ml] were higher in high BNP group than those in low BNP group both in 10 and 12 weeks post-operation ( P =0.013, P =0.013, P =0.002, respectively).Con-clusions PRA was increased in dogs with CHF and associated with the severity of CHF.%目的:探讨肾交感神经活性与慢性心力衰竭(简称心衰)犬心衰严重程度间关系。方法采用腹主动脉结扎的方法建立犬慢性心衰模型,观察术后不同时间心衰犬(9只)与对照组(3只)以及不同严重程度心衰组间血浆肾素活性( PRA)、肾上腺素( E)及去甲肾上腺素( NE)的差异。结果与对照组相比,术后第10和12周心衰犬脑钠尿肽( BNP)增高,血浆E、NE、PRA增加( P均<0.01)。与术后10周组相比,术后12周组PRA[(2.26±0.16)ng/(ml・ h) vs (2.08±0.08)ng/(ml・ h)]、NE[(202.99±16

  3. Assessment of cardiac sympathetic nerve abnormalities by {sup 123}I-MIBG (metaiodobenzylguanidine) myocardial scintigraphy in diabetic patients undergoing hemodialysis

    Energy Technology Data Exchange (ETDEWEB)

    Ohashi, Hiroshige; Oda, Hiroshi; Matsuno, Yukihiko [Prefectural Gifu Hospital (Japan)] [and others

    1995-05-01

    We compared cardiac sympathetic nerve abnormalities in patients hemodialyzed because of diabetic nephropathy (DN, n=18) and chronic glomerulonephritis (CGN, n=21). {sup 123}I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy was performed in this study. SPECT and anterior planar myocardial images were obtained 15 minutes after (initial images) and 4 hours after (delayed images) an injection of MIBG. The following results were obtained: (1) SPECT showed more defects in DN than in CGN. (2) The heart to superior mediastinum uptake ratio (H/M) was lower in DN than in CGN. These findings suggest that myocardial uptake of MIBG in DN is significantly impaired because of cardiac sympathetic nerve abnormalities. These abnormalities may affect the prognosis in DN. (author).

  4. Slow and deep respiration suppresses steady-state sympathetic nerve activity in patients with chronic heart failure: from modeling to clinical application.

    Science.gov (United States)

    Harada, Daisuke; Asanoi, Hidetsugu; Takagawa, Junya; Ishise, Hisanari; Ueno, Hiroshi; Oda, Yoshitaka; Goso, Yukiko; Joho, Shuji; Inoue, Hiroshi

    2014-10-15

    Influences of slow and deep respiration on steady-state sympathetic nerve activity remain controversial in humans and could vary depending on disease conditions and basal sympathetic nerve activity. To elucidate the respiratory modulation of steady-state sympathetic nerve activity, we modeled the dynamic nature of the relationship between lung inflation and muscle sympathetic nerve activity (MSNA) in 11 heart failure patients with exaggerated sympathetic outflow at rest. An autoregressive exogenous input model was utilized to simulate entire responses of MSNA to variable respiratory patterns. In another 18 patients, we determined the influence of increasing tidal volume and slowing respiratory frequency on MSNA; 10 patients underwent a 15-min device-guided slow respiration and the remaining 8 had no respiratory modification. The model predicted that a 1-liter, step increase of lung volume decreased MSNA dynamically; its nadir (-33 ± 22%) occurred at 2.4 s; and steady-state decrease (-15 ± 5%), at 6 s. Actually, in patients with the device-guided slow and deep respiration, respiratory frequency effectively fell from 16.4 ± 3.9 to 6.7 ± 2.8/min (P state MSNA was decreased by 31% (P state MSNA. Thus slow and deep respiration suppresses steady-state sympathetic nerve activity in patients with high levels of resting sympathetic tone as in heart failure.

  5. Identification of M1 muscarinic receptors in pulmonary sympathetic nerves in the guinea-pig by use of pirenzepine.

    Science.gov (United States)

    Maclagan, J.; Fryer, A. D.; Faulkner, D.

    1989-01-01

    1. The effect of pirenzepine, a muscarinic antagonist considered to be selective for M1 receptors, was studied on bronchoconstriction and bradycardia elicited by preganglionic stimulation of the parasympathetic vagal nerves and by i.v. injections of acetylcholine (ACh) in anaesthetized guinea-pigs. 2. Pirenzepine was equipotent in the heart and lung as an antagonist of the effects of i.v. ACh at postjunctional muscarinic receptors. Doses of pirenzepine in excess of 1 mumol kg-1 abolished all muscarinic responses consistent with non-selective blockade of M3 receptors on airway smooth muscle and M2 receptors on atrial cells. 3. In the lung, low doses of pirenzepine (1-100 nmol kg-1) increased vagally-induced bronchoconstriction despite concurrent partial blockade of the postjunctional receptors. This suggests blockade of neuronal muscarinic receptors. 4. Propranolol (1 mg kg-1) increased control bronchoconstrictor responses elicited by ACh and vagal stimulation but did not alter the potency of pirenzepine for postjunctional receptors in heart or lung. However, pirenzepine-induced enhancement of vagally-induced bronchoconstriction was abolished by propranolol, suggesting that pirenzepine may be an antagonist for muscarinic receptors located in the sympathetic nerves innervating airway smooth muscle. 5. These results confirm that bronchoconstrictor stimuli indirectly initiate activation of an opposing sympathetic reflex in the guinea-pig lung. This response is facilitated by muscarinic receptors located in the sympathetic nervous pathway. 6. The high potency of pirenzepine for the neuronal receptors in the sympathetic nerves suggests that these are M1 receptors. In contrast, the parasympathetic nerves innervating airway smooth muscle in this species contain M2 receptors which inhibit neurotransmission. PMID:2758228

  6. The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats.

    Directory of Open Access Journals (Sweden)

    Jie Song

    Full Text Available During hypovolemic shock, skeletal muscle blood flow could be redistributed to vital organs via vasoconstriction in part evoked by activation of the innervating sympathetic nerve activity. However, it is not well known whether this mechanism operates during anaphylactic shock. We determined the femoral artery blood flow (FBF and lumbar sympathetic nerve activity (LSNA mainly regulating the hindquater muscle blood flow during anaphylactic hypotension in anesthetized rats. Anesthetized Sprague-Dawley rats were randomly allocated to the following groups (n = 7/group: (1 non-sensitized, (2 anaphylaxis, (3 anaphylaxis-lumbar sympathectomy (LS and (4 anaphylaxis-sinoaortic denervation (SAD groups. Anaphylaxis was induced by an intravenous injection of the ovalbumin antigen to the sensitized rats. The systemic arterial pressure (SAP, heart rate (HR, central venous pressure (CVP, FBF and LSNA were continuously measured. In the anaphylaxis group, LSNA and HR increased, while SAP and FBF decreased after antigen injection. In the anaphylaxis-SAD group, LSNA did not significantly change during the early phase, but the responses of SAP and FBF were similar to those in the anaphylaxis group. In the anaphylaxis-LS group, both FBF and SAP decreased similarly to the anaphylaxis group during anaphylactic hypotension. These results indicated that LSNA increased via baroreceptor reflex, but this sympathoexcitation or LS did not affect antigen-induced decreases in FBF or SAP. Lumbar sympathetic nerves are not involved in regulation of the blood flow to the hindlimb or systemic blood pressure during anaphylactic hypotension in anesthetized rats.

  7. Skin sympathetic nerve activity in humans during exposure to emotionally-charged images: sex differences

    Directory of Open Access Journals (Sweden)

    Rachael eBrown

    2014-03-01

    Full Text Available While it is known that anxiety or emotional arousal affects skin sympathetic nerve activity (SSNA, the galvanic skin response (GSR is the most widely used parameter to infer increases in SSNA during stress or emotional studies. We recently showed that SSNA provides a more sensitive measure of emotional state than effector-organ responses. The aim of the present study was to assess whether there are gender differences in the responses of SSNA and other physiological parameters such as blood pressure, heart rate, skin blood flow and sweat release, while subjects viewed neutral or emotionally-charged images from the International Affective Picture System. Changes in SSNA were assessed using microneurography in twenty subjects (ten male and ten female. Blocks of positively-charged (erotica or negatively-charge images (mutilation were presented in a quasi-random fashion, following a block of neutral images, with each block containing fifteen images and lasting two minutes. Images of both erotica and mutilation caused significant increases in SSNA, with increases being greater for males viewing erotica and greater for females viewing mutilation. The increases in SSNA were often coupled with sweat release and cutaneous vasoconstriction; however, these markers were not significantly different than those produced by viewing neutral images and were not always consistent with the SSNA increases. We conclude that SSNA increases with both positively-charged and negatively-charged emotional images, yet sex differences are present.

  8. Baroreflex modulation of muscle sympathetic nerve activity during cold pressor test in humans

    Science.gov (United States)

    Cui, Jian; Wilson, Thad E.; Crandall, Craig G.

    2002-01-01

    The purpose of this project was to test the hypothesis that baroreceptor modulation of muscle sympathetic nerve activity (MSNA) and heart rate is altered during the cold pressor test. Ten subjects were exposed to a cold pressor test by immersing a hand in ice water for 3 min while arterial blood pressure, heart rate, and MSNA were recorded. During the second and third minute of the cold pressor test, blood pressure was lowered and then raised by intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure was more negative (P cold pressor test (-244.9 +/- 26.3 units x beat(-1) x mmHg(-1)) when compared with control conditions (-138.8 +/- 18.6 units x beat(-1) x mmHg(-1)), whereas no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that baroreceptors remain capable of modulating MSNA and heart rate during a cold pressor test; however, the sensitivity of baroreflex modulation of MSNA is elevated without altering the sensitivity of baroreflex control of heart rate.

  9. Arbitrary units are a composite and useful measure of muscle sympathetic nerve activity.

    Science.gov (United States)

    Thakre, Tushar P; Kulkarni, Hemant; Mamtani, Manju R; Smith, Michael

    2009-08-01

    In humans, the muscle sympathetic nerve activity (MSNA) signal is challenging to detect, record and analyze. Several methods exist that attempt to capture the latent construct of MSNA. We directly compared the performance of five MSNA parameters: burst frequency, burst incidence, median burst amplitude, arbitrary units (AU) and fractal dimension (FD). The MSNA signal was recorded in 33 subjects for approximately 30 min before, during and after the application of a graded cold pressor test stimulus at 18 degrees C, 10 degrees C and 2 degrees C in random order with an adequate wash-out period. Using coefficient of variation, Shannon's entropy and principal component analysis, we observed that these five parameters defined two physical and conceptual domains of MSNA-frequency and amplitude. Since AU combines information from both these domains, we observed that it explained maximum inter-subject and inter-experimental segment variation. FD did not explain the inter-subject variability and was identified as a unique parameter in the factor analysis. Epidemiological studies that attempt to quantify MSNA may consistently use AU as the parameter for quantification of MSNA.

  10. The Cardiac Sympathetic Nerve Activity in the Elderly Is Attenuated in the Right Lateral Decubitus Position

    Science.gov (United States)

    Sasaki, Konosuke; Haga, Mayu; Bao, Sarina; Sato, Haruka; Saiki, Yoshikatsu; Maruyama, Ryoko

    2017-01-01

    Objectives: The aim of this study was to evaluate the effect of the supine, left lateral decubitus, and right lateral decubitus positions on autonomic nervous activity in elderly adults by using spectral analysis of heart rate variability (HRV). Method: Forty-five adults aged 73.6 ± 5.7 years were enrolled. After lying in the supine position, all participants moved to the lateral decubitus positions in a random order and maintained the positions for 10 min, while electrocardiographic data were recorded to measure HRV. Results: The lowest heart rate continued for 10 min when participants were in the left lateral decubitus position compared with the other two positions (p < .001), while the HRV indexes remained unchanged. The low-frequency HRV to high-frequency HRV ratio (LF/HF) for the right lateral decubitus position was significantly lower than that for the other positions. Discussion: The right lateral decubitus position may attenuate sympathetic nerve activity in elderly adults. PMID:28516131

  11. Muscle sympathetic nerve responses to physiological changes in prostaglandin production in humans

    Science.gov (United States)

    Doerzbacher, K. J.; Ray, C. A.

    2001-01-01

    Previous studies suggest that prostaglandins may contribute to exercise-induced increases in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA was measured at rest and during exercise before and after oral administration of ketoprofen, a cyclooxygenase inhibitor, or placebo. Twenty-one subjects completed two bouts of graded dynamic and isometric handgrip to fatigue. Each exercise bout was followed by 2 min of postexercise muscle ischemia. The second exercise bouts were performed after 60 min of rest in which 11 subjects were given ketoprofen (300 mg) and 10 subjects received a placebo. Ketoprofen significantly lowered plasma thromboxane B(2) in the drug group (from 36 +/- 6 to 22 +/- 3 pg/ml, P muscle ischemia. There was no relationship between thromboxane B(2) concentrations and MSNA or arterial pressure responses during both exercise modes. The data indicate that physiological increases or decreases in prostaglandins do not alter exercise-induced increases in MSNA and arterial pressure in humans. These findings suggest that contraction-induced metabolites other than prostaglandins mediate MSNA responses to exercise in humans.

  12. Baroreflex modulation of muscle sympathetic nerve activity during posthandgrip muscle ischemia in humans

    Science.gov (United States)

    Cui, J.; Wilson, T. E.; Shibasaki, M.; Hodges, N. A.; Crandall, C. G.

    2001-01-01

    To identify whether muscle metaboreceptor stimulation alters baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA, beat-by-beat arterial blood pressure (Finapres), and electrocardiogram were recorded in 11 healthy subjects in the supine position. Subjects performed 2 min of isometric handgrip exercise at 40% of maximal voluntary contraction followed by 2.5 min of posthandgrip muscle ischemia. During muscle ischemia, blood pressure was lowered and then raised by intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure was more negative (P ischemia (-201.9 +/- 20.4 units. beat(-1). mmHg(-1)) when compared with control conditions (-142.7 +/- 17.3 units. beat(-1). mmHg(-1)). No significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. However, both curves shifted during postexercise ischemia to accommodate the elevation in blood pressure and MSNA that occurs with this condition. These data suggest that the sensitivity of baroreflex modulation of MSNA is elevated by muscle metaboreceptor stimulation, whereas the sensitivity of baroreflex of modulate heart rate is unchanged during posthandgrip muscle ischemia.

  13. The posterior vermis of the cerebellum selectively inhibits 10-Hz sympathetic nerve discharge in anesthetized cats.

    Science.gov (United States)

    Barman, Susan M; Gebber, Gerard L

    2009-07-01

    We studied the changes in inferior cardiac sympathetic nerve discharge (SND) and mean arterial pressure (MAP) produced by aspiration or chemical inactivation (muscimol microinjection) of lobule IX (uvula) of the posterior vermis of the cerebellum in baroreceptor-denervated and baroreceptor-innervated cats anesthetized with urethane. Autospectral analysis was used to decompose SND into its frequency components. Special attention was paid to the question of whether the experimental procedures affected the rhythmic (10-Hz and cardiac-related) components of SND. Aspiration or chemical inactivation of lobule IX produced an approximately three-fold increase in the 10-Hz rhythmic component of SND (P cats. Total power (0- to 20-Hz band) was unchanged. Despite the absence of a change in total power in SND, there was a statistically significant increase in MAP. In baroreceptor-innervated cats, neither aspiration nor chemical inactivation of the uvula caused a significant change in cardiac-related or total power in SND or MAP. These results are the first to demonstrate a role of cerebellar cortical neurons of the posterior vermis in regulating the frequency composition of naturally occurring SND. Specifically, these neurons selectively inhibit the 10-Hz rhythm-generating network in baroreceptor-denervated, urethane-anesthetized cats. The functional implications of these findings are discussed.

  14. Renal sympathetic denervation prevents the development of pulmonary arterial hypertension and cardiac dysfunction in dogs.

    Science.gov (United States)

    Hu, Wei; Yu, Sheng-Bo; Chen, Liao; Guo, Rui-Qiang; Zhao, Qing-Yan

    2015-08-01

    The renin-angiotensin-aldosterone system is activated in pulmonary arterial hypertension (PAH) patients, and this activation may have long-term negative effects on the progression of PAH. The purpose of this study was to evaluate the effects of transcatheter renal sympathetic denervation (RSD) on the development of pulmonary arterial hypertension and cardiac dysfunction in dogs using two-dimensional speckle tracking imaging. Twenty-two dogs were randomly divided into three groups: control group (n = 7), PAH group (n = 8), and PAH + RSD group (n = 7). All dogs were assessed using two-dimensional speckle tracking imaging. The ventricular strain, ventricular synchrony, left ventricular (LV) twist, and torsion rate were analyzed to evaluate cardiac function. After 8 weeks, the right ventricular lateral longitudinal strain and the septum longitudinal strain were reduced in the PAH group compared with the control group (p dogs.

  15. Sympathetic nerve damage and restoration after ischemia-reperfusion injury as assessed by {sup 11}C-hydroxyephedrine

    Energy Technology Data Exchange (ETDEWEB)

    Werner, Rudolf A.; Higuchi, Takahiro [University of Wuerzburg, Department of Nuclear Medicine, Wuerzburg (Germany); University of Wuerzburg, Comprehensive Heart Failure Center, Wuerzburg (Germany); Maya, Yoshifumi [University of Wuerzburg, Department of Nuclear Medicine, Wuerzburg (Germany); Nihon Medi-Physics Co., Ltd., Research Centre, Chiba (Japan); Rischpler, Christoph [Technische Universitaet Muenchen, Department of Nuclear Medicine, Klinikum rechts der Isar, Muenchen (Germany); Javadi, Mehrbod S. [Johns Hopkins University, Division of Nuclear Medicine, Russell H. Morgan Department of Radiology, Baltimore, MD (United States); Fukushima, Kazuhito [Hyogo College of Medicine, Department of Radiology, Hyogo (Japan); Lapa, Constantin [University of Wuerzburg, Department of Nuclear Medicine, Wuerzburg (Germany); Herrmann, Ken [University of Wuerzburg, Department of Nuclear Medicine, Wuerzburg (Germany); David Geffen School of Medicine at UCLA, Department of Molecular and Medical Pharmacology, Los Angeles, CA (United States)

    2016-02-15

    An altered state of the cardiac sympathetic nerves is an important prognostic factor in patients with coronary artery disease. The aim of this study was to investigate regional sympathetic nerve damage and restoration utilizing a rat model of myocardial transient ischemia and a catecholamine analog PET tracer, {sup 11}C-hydroxyephedrine ({sup 11}C-HED). Transient myocardial ischemia was induced by coronary occlusion for 20 min and reperfusion in male Wistar rats. Dual-tracer autoradiography was performed subacutely (7 days) and chronically (2 months) after ischemia, and in control rats without ischemia using {sup 11}C-HED as a marker of sympathetic innervation and {sup 201}TI for perfusion. Additional serial in vivo cardiac {sup 11}C-HED and {sup 18}F-FDG PET scans were performed in the subacute and chronic phases after ischemia. After transient ischemia, the {sup 11}C-HED uptake defect areas in both the subacute and chronic phases were clearly larger than the perfusion defect areas in the midventricular wall. The subacute {sup 11}C-HED uptake defect showed a transmural pattern, whereas uptake recovered in the subepicardial portion in the chronic phase. Tyrosine hydroxylase antibody nerve staining confirmed regional denervation corresponding to areas of decreased {sup 11}C-HED uptake. Serial in vivo PET imaging visualized reductions in the area of the {sup 11}C-HED uptake defects in the chronic phase consistent with autoradiography and histology. Higher susceptibility of sympathetic neurons compared to myocytes was confirmed by a larger {sup 11}C-HED defect with a corresponding histologically identified region of denervation. Furthermore, partial reinnervation was observed in the chronic phase as shown by recovery of subepicardial {sup 11}C-HED uptake. (orig.)

  16. A technique for estimating activity in whole nerve trunks applied to the cervical sympathetic trunk, in the rabbit.

    Science.gov (United States)

    Hellström, F; Roatta, S; Johansson, H; Passatore, M

    1999-12-24

    The changes in sympathetic outflow may be evaluated from the amplitude of the antidromic compound action potential (ACAP) according to the collision technique described by Douglas and Ritchie (Douglas, W.W. and Ritchie J.M., A technique for recording functional activity in specific groups of medullated and non-medullated fibers in whole nerve trunks. J. Physiol., 138(1957) 19-30). This technique was revised, taking into account the depressant action exerted by antidromic stimulation on sympathetic preganglionic neurones (SPNs). Cervical sympathetic nerve (CSN) of rabbits was used as experimental model. Stimulation frequencies of 0.2-0.5 Hz were found to be sufficiently low to avoid depressant actions on CSN spontaneous activity; they were employed to test the sensitivity of the technique during different experimental manoeuvres, such as changes in pulmonary-ventilation, baroreceptor unloading and arousal stimuli. In addition a procedure was devised to calibrate the ACAP amplitude: high frequency antidromic stimulation was used to induce a complete and transient inhibition of SPNs which allows to record the ACAP maximum amplitude. ACAPs recorded in various experimental conditions can then be expressed as percentage of this value.

  17. Clinical usefulness of {sup 123}I-metaiodobenzylguanidine myocardial scintigraphy in diabetic patients with cardiac sympathetic nerve dysfunction

    Energy Technology Data Exchange (ETDEWEB)

    Miyanaga, Hajime; Yoneyama, Satoshi; Kamitani, Tadaaki; Kawasaki, Shingo; Takahashi, Toru; Kunishige, Hiroshi [Matsushita Memorial Hospital, Osaka (Japan)

    1995-09-01

    To assess the clinical utility of {sup 123}I-metaiodobenzylguanidine (MIBG) scintigraphy in evaluating cardiac sympathetic nerve disturbance in diabetic patients, we performed MIBG scintigraphy in 18 diabetic patients and 11 normal controls. Diabetic patients with symptomatic neuropathy (DM2) had a significantly lower heart to mediastinum uptake ratio than did those without neuropathy or normal controls in initial and delayed images (initial image, 1.90{+-}0.27 vs 2.32{+-}0.38, 2.41{+-}0.40, p<0.01; delayed image, 1.80{+-}0.31 vs 2.48{+-}0.35, 2.56{+-}0.28, p<001, respectively). Defect score, assessed visually, were higher in DM2 patients than in patients in the other two groups (initial image, 7{+-}2.6 vs 1.5{+-}1.9, 0.7{+-}0.9; delayed image 10.6{+-}3.3 vs 4.0{+-}2.5, 1.7{+-}1.6 p<0.01, respectively). The maximum washout rate in DM2 patients was also higher than those in patients in the other two groups. The findings of these indices obtained from MIBG scintigraphy coincided with the % low-frequency power extracted from heart rate fluctuations using a power spectral analysis and the results of the Schellong test, which were used to evaluate sympathetic function. These results suggest that MIBG scintigraphy may be useful for evaluating cardiac sympathetic nerve disturbance in patients with diabetes. (author).

  18. Role of endothelin-1 in mediating changes in cardiac sympathetic nerve activity in heart failure.

    Science.gov (United States)

    Abukar, Yonis; May, Clive N; Ramchandra, Rohit

    2016-01-01

    Heart failure (HF) is associated with increased sympathetic nerve activity to the heart (CSNA), which is directly linked to mortality in HF patients. Previous studies indicate that HF is associated with high levels of plasma endothelin-1 (ET-1), which correlates with the severity of the disease. We hypothesized that blockade of endothelin receptors would decrease CSNA. The effects of intravenous tezosentan (a nonselective ETA and ETB receptor antagonist) (8 mg·kg(-1)·h(-1)) on resting levels of CSNA, arterial pressure, and heart rate were determined in conscious normal sheep (n = 6) and sheep with pacing-induced HF (n = 7). HF was associated with a significant decrease in ejection fraction (from 74 ± 2% to 38 ± 1%, P < 0.001) and a significant increase in resting levels of CSNA burst incidence (from 56 ± 11 to 87 ± 2 bursts/100 heartbeats, P < 0.01). Infusion of tezosentan for 60 min significantly decreased resting mean aterial pressure (MAP) in both normal and HF sheep (-8 ± 4 mmHg and -4 ± 3 mmHg, respectively; P < 0.05). This was associated with a significant decrease in CSNA (by 25 ± 26% of control) in normal sheep, but there was no change in CSNA in HF sheep. Calculation of spontaneous baroreflex gain indicated significant impairment of the baroreflex control of HR after intravenous tezosentan infusion in normal animals but no change in HF animals. These data suggest that endogenous levels of ET-1 contribute to the baseline levels of CSNA in normal animals, but this effect is absent in HF.

  19. Cardiac sympathetic nerve abnormality predicts ventricular tachyarrhythmic events in patients without conventional risk of sudden death.

    Science.gov (United States)

    Akutsu, Yasushi; Kaneko, Kyouichi; Kodama, Yusuke; Li, Hui-Ling; Kawamura, Mitsuharu; Asano, Taku; Tanno, Kaoru; Shinozuka, Akira; Gokan, Takehiko; Kobayashi, Youichi

    2008-11-01

    Patients with structural heart disease, severe left ventricular dysfunction, or history of cardiac arrest are at increased risk of sudden cardiac death. However, a useful marker for predicting sudden cardiac death is not clarified in low-risk patients without those conventional risks. We hypothesized that cardiac sympathetic nerve system (SNS) abnormality would be associated with ventricular tachyarrhythmic events in low-risk patients with ventricular tachycardia (VT). Iodine-123 metaiodobenzylguanidine ((123)I-MIBG) scintigraphy was performed in 50 patients (mean+/-standard deviation, age 54 +/- 16 years, 52% males) with VT who did not have structural heart disease, severe left ventricular dysfunction, or history of cardiac arrest, and SNS activity was assessed from heart/mediastinal (H/M) ratio on delayed images. Over 11 years of follow-up, three patients had sudden deaths (6%) and nine patients had sustained ventricular tachyarrhythmic events (18%). SNS abnormality, defined as H/M ratio SNS abnormality vs 16.7% in three of 30 patients without SNS abnormality, p = 0.005). After adjustment for potential confounding variables including slight left ventricular dysfunction, SNS abnormality remained independently predictive of ventricular tachyarrhythmic events with a hazard ratio of 5.3 (95% confidence interval = 1.4 to 20.8, p = 0.016). SNS abnormality is a readily available and powerful predictor of recurrent ventricular tachyarrhythmic events in patients with VT who did not have conventional risk of sudden cardiac death. (123)I-MIBG scintigraphy can provide prognostic information of VT patients without conventional risk.

  20. Cardiac sympathetic nerve abnormality predicts ventricular tachyarrhythmic events in patients without conventional risk of sudden death

    Energy Technology Data Exchange (ETDEWEB)

    Akutsu, Yasushi; Kaneko, Kyouichi; Kodama, Yusuke; Li, Hui-Ling; Kawamura, Mitsuharu; Asano, Taku; Tanno, Kaoru; Kobayashi, Youichi [Showa University School of Medicine, Division of Cardiology, Department of Medicine, Tokyo (Japan); Shinozuka, Akira; Gokan, Takehiko [Showa University School of Medicine, Department of Radiology, Tokyo (Japan)

    2008-11-15

    Patients with structural heart disease, severe left ventricular dysfunction, or history of cardiac arrest are at increased risk of sudden cardiac death. However, a useful marker for predicting sudden cardiac death is not clarified in low-risk patients without those conventional risks. We hypothesized that cardiac sympathetic nerve system (SNS) abnormality would be associated with ventricular tachyarrhythmic events in low-risk patients with ventricular tachycardia (VT). Iodine-123 metaiodobenzylguanidine ({sup 123}I-MIBG) scintigraphy was performed in 50 patients (mean{+-}standard deviation, age 54 {+-} 16 years, 52% males) with VT who did not have structural heart disease, severe left ventricular dysfunction, or history of cardiac arrest, and SNS activity was assessed from heart/mediastinal (H/M) ratio on delayed images. Over 11 years of follow-up, three patients had sudden deaths (6%) and nine patients had sustained ventricular tachyarrhythmic events (18%). SNS abnormality, defined as H/M ratio <2.8, was predictive of sudden death or ventricular tachyarrhythmic events (45% in nine of 20 patients with SNS abnormality vs 16.7% in three of 30 patients without SNS abnormality, p = 0.005). After adjustment for potential confounding variables including slight left ventricular dysfunction, SNS abnormality remained independently predictive of ventricular tachyarrhythmic events with a hazard ratio of 5.3 (95% confidence interval = 1.4 to 20.8, p = 0.016). SNS abnormality is a readily available and powerful predictor of recurrent ventricular tachyarrhythmic events in patients with VT who did not have conventional risk of sudden cardiac death. {sup 123}I-MIBG scintigraphy can provide prognostic information of VT patients without conventional risk. (orig.)

  1. Matured Hop Bittering Components Induce Thermogenesis in Brown Adipose Tissue via Sympathetic Nerve Activity.

    Directory of Open Access Journals (Sweden)

    Yumie Morimoto-Kobayashi

    Full Text Available Obesity is the principal symptom of metabolic syndrome, which refers to a group of risk factors that increase the likelihood of atherosclerosis. In recent decades there has been a sharp rise in the incidence of obesity throughout the developed world. Iso-α-acids, the bitter compounds derived from hops in beer, have been shown to prevent diet-induced obesity by increasing lipid oxidation in the liver and inhibition of lipid absorption from the intestine. Whereas the sharp bitterness induced by effective dose of iso-α-acids precludes their acceptance as a nutrient, matured hop bittering components (MHB appear to be more agreeable. Therefore, we tested MHB for an effect on ameliorating diet-induced body fat accumulation in rodents. MHB ingestion had a beneficial effect but, compared to iso-α-acids and despite containing structurally similar compounds, acted via different mechanisms to reduce body fat accumulation. MHB supplementation significantly reduced body weight gain, epididymal white adipose tissue weight, and plasma non-esterified free fatty acid levels in diet-induced obese mice. We also found that uncoupling protein 1 (UCP1 expression in brown adipose tissue (BAT was significantly increased in MHB-fed mice at both the mRNA and protein levels. In addition, MHB administration in rats induced the β-adrenergic signaling cascade, which is related to cAMP accumulation in BAT, suggesting that MHB could modulate sympathetic nerve activity innervating BAT (BAT-SNA. Indeed, single oral administration of MHB elevated BAT-SNA in rats, and this elevation was dissipated by subdiaphragmatic vagotomy. Single oral administration of MHB maintained BAT temperature at a significantly higher level than in control rats. Taken together, these findings indicate that MHB ameliorates diet-induced body fat accumulation, at least partly, by enhancing thermogenesis in BAT via BAT-SNA activation. Our data suggests that MHB is a useful tool for developing functional

  2. 超声能源在去肾交感治疗中的应用%Application of Ultrasound in Renal Sympathetic Denervation

    Institute of Scientific and Technical Information of China (English)

    黄晶

    2014-01-01

    Renal sympathetic denervation (RDN) with radiofrequency energy is a novel therapeutic technique for the treatment of patients with resistant hypertension. Nevertheless, radiofrequency ablation of renal sympathetic nerves bears numerous disadvantages, e.g., low efifciency;patient’s suffering from pain during ablation and unresponsiveness to the treatment, as well as successful procedural performance depending on the type of target vessels, etc. While ultrasound, when longitudinally propagating through the biological tissue, may cause the medium molecules to vibrate violently, with subsequent generation of mechanical friction, cavitation and thermal effects; thus, can be applied for RDN. Compared with radiofrequency energy, it has many advantages in terms of safety and efifcacy. This review is about the-state-of-art of ultrasound ablation for renal sympathetic nerves.%以SymplicityTM 为代表的利用射频能量行去肾交感神经术开创了经皮血管介入治疗顽固性高血压的全新途径。但射频能量消融尚存在消融效率较低、消融时患者疼痛明显、部分患者对治疗无反应(约20%)及完成治疗过程依耐于标准的患者血管类型等缺点。而超声作为一种频率高于听阈的机械波,在生物组织中以纵波传播时,其携带的机械能可使介质中的分子剧烈震荡产生机械摩擦、空化和热效应等,因此可用于去肾交感神经术。且与射频能量消融相比,超声能量在安全性和有效性方面有诸多优势。本综述即将对经导管超声消融肾交感神经相关研究进展作一系统阐述。

  3. Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland.

    Science.gov (United States)

    Ziółkowska, N; Lewczuk, B; Przybylska-Gornowicz, B

    2015-01-01

    Norepinephrine (NE) released from the sympathetic nerve endings is the main neurotransmitter controlling melatonin synthesis in the mammalian pineal gland. Although neuropeptide Y (NPY) co-exists with NE in the pineal sympathetic nerve fibers it also occurs in a population of non-adrenergic nerve fibers located in this gland. The role of NPY in pineal physiology is still enigmatic. The present study characterizes the effect of NPY on the depolarization-evoked 3H-NE release from the pig pineal explants. The explants of the pig pineal gland were loaded with 3H-NE in the presence of pargyline and superfused with Tyrode medium. They were exposed twice to the modified Tyrode medium containing 60 mM of K+ to evoke the 3H-NE release via depolarization. NPY, specific agonists of Y1- and Y2- receptors and pharmacologically active ligands of α2-adrenoceptors were added to the medium before and during the second depolarization. The radioactivity was measured in medium fractions collected every 2 minutes during the superfusion. NPY (0.1-10 μM) significantly decreased the depolarization-induced 3H-NE release. Similar effect was observed after the treatment with Y2-agonist: NPY13-36, but not with Y1-agonist: [Leu31,Pro34]-NPY. The tritium overflow was lower in the explants exposed to the 5 μM NPY and 1 μM rauwolscine than to rauwolscine only. The effects of 5 μM NPY and 0.05 μM UK 14,304 on the depolarization-evoked 3H-NE release were additive. The results show that NPY is involved in the regulation of NE release from the sympathetic terminals in the pig pineal gland, inhibiting this process via Y2-receptors.

  4. Low-frequency physiological activation of the vestibular utricle causes biphasic modulation of skin sympathetic nerve activity in humans.

    Science.gov (United States)

    Grewal, Tarandeep; Dawood, Tye; Hammam, Elie; Kwok, Kenny; Macefield, Vaughan G

    2012-07-01

    We have previously shown that sinusoidal galvanic vestibular stimulation, a means of selectively modulating vestibular afferent activity, can cause partial entrainment of sympathetic outflow to muscle and skin in human subjects. However, it influences the firing of afferents from the entire vestibular apparatus, including the semicircular canals. Here, we tested the hypothesis that selective stimulation of one set of otolithic organs-those located in the utricle, which are sensitive to displacement in the horizontal axis-could entrain sympathetic nerve activity. Skin sympathetic nerve activity (SSNA) was recorded via tungsten microelectrodes inserted into cutaneous fascicles of the common peroneal nerve in 10 awake subjects, seated (head vertical, eyes closed) on a motorised platform. Slow sinusoidal accelerations-decelerations (~4 mG) were applied in the X (antero-posterior) or Y (medio-lateral) direction at 0.08 Hz; composite movements in both directions were also applied. Subjects either reported feeling a vague sense of movement (with no sense of direction) or no movement at all. Nevertheless, cross-correlation analysis revealed a marked entrainment of SSNA for all types of movements: vestibular modulation was 97 ± 3 % for movements in the X axis and 91 ± 5 % for displacements in the Y axis. For each sinusoidal cycle, there were two major peaks of modulation-one associated with acceleration as the platform moved forward or to the side, and one associated with acceleration in the opposite direction. We interpret these observations as reflecting inertial displacement of the stereocilia within the utricle during acceleration, which causes a robust vestibulosympathetic reflex.

  5. Exercise training to reduce sympathetic nerve activity in heart failure patients. A systematic review and meta-analysis.

    Science.gov (United States)

    Saavedra, María Javiera; Romero, Fernando; Roa, Jorge; Rodríguez-Núñez, Iván

    2017-07-07

    To determine the effects of exercise training on sympathetic nerve activity in heart failure patients. A systematic review was performed. An electronic search of MEDLINE, ProQuest, SciELO, SPORTDiscus, Rehabilitation and Sport Medicine Source, Cumulative Index to Nursing and Allied Health Literature, Tripdatabase, Science Direct and PEDrO was performed from their inception to February 2017. Clinical trials and quasi-experimental studies were considered for primary article selection. The studies should include patients diagnosed with chronic heart failure that performed exercise training for at least 4 weeks. Sympathetic nerve activity should be measured by microneurography before and after the intervention. The Cochrane Collaboration's Risk of Bias Tool was used to evaluate risk of bias, and the quality of evidence was rated following the GRADE approach. Standardized mean differences (SMD) were calculated for control and experimental groups. Meta-analysis was performed using the random effects model. Five trials were included. Overall, the trials had moderate risk of bias. The experimental group indicated a significant decrease in the number of bursts per minute (SMD -2.48; 95% CI -3.55 to -1.41) when compared to the control group. Meanwhile, a significant decrease was also observed in the prevalence of bursts per 100 beats in the experimental group when compared to the control group (SMD -2.66; 95% CI -3.64 to -1.69). Exercise training could be effective in reducing sympathetic nerve activity in patients with heart failure. The quality of evidence across the studies was moderate. Future studies are necessary to confirm these results. Copyright © 2017 Associação Brasileira de Pesquisa e Pós-Graduação em Fisioterapia. Publicado por Elsevier Editora Ltda. All rights reserved.

  6. Effect of stimulation of afferent renal nerves on plasma levels of vasopressin

    Energy Technology Data Exchange (ETDEWEB)

    Caverson, M.M.; Ciriello, J.

    1987-04-01

    Experiments were done in ..cap alpha..-chloralose-anesthetized, paralyzed and artificially ventilated cats with vagus, cervical sympathetic, aortic depressor, and carotid sinus nerves cut bilaterally to investigate the effect of afferent renal nerve (ARN) stimulation on circulating levels of vasopressin (AVP). Electrical stimulation of ARN elicited a pressor response that had two components, a primary (1/sup 0/) component locked in time with the stimulus and a secondary (2/sup 0/) component that had a long onset latency and that outlasted the stimulation period. The 1/sup 0/ and 2/sup 0/ components of the pressor response were largest at stimulation frequencies of 30 and 40 Hz, respectively. Autonomic blockage with hexamethonium bromide and atropine methylbromide abolished the 1/sup 0/ component. Administration of the vasopressin V/sub 1/-vascular receptor antagonist d(CH/sub 2/)/sub 5/ VAVP during autonomic blockade abolished the 2/sup 0/C component. Plasma concentrations of AVP measured by radioimmunoassay increased from control levels of 5.2 +/- 0.9 to 53.6 +/- 18.6 pg/ml during a 5-min period of stimulation of ARN. Plasma AVP levels measured 20-40 min after simulation were not significantly different from control values. These data demonstrate that sensory information originating in the kidney alters the release of vasopressin from the neurohypophysis and suggest that ARN are an important component of the neural circuitry involved in homeostatic mechanisms controlling arterial pressure.

  7. Sex differences in ischemia/reperfusion-induced acute kidney injury are dependent on the renal sympathetic nervous system.

    Science.gov (United States)

    Tanaka, Ryosuke; Tsutsui, Hidenobu; Ohkita, Mamoru; Takaoka, Masanori; Yukimura, Tokihito; Matsumura, Yasuo

    2013-08-15

    Resistance to ischemic acute kidney injury has been shown to be higher in female rats than in male rats. We found that renal venous norepinephrine overflow after reperfusion played important roles in the development of ischemic acute kidney injury. In the present study, we investigated whether sex differences in the pathogenesis of ischemic acute kidney injury were derived from the renal sympathetic nervous system using male and female Sprague-Dawley rats. Ischemia/reperfusion-induced acute kidney injury was achieved by clamping the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function was impaired after reperfusion in both male and female rats; however, renal dysfunction and histological damage were more severe in male rats than in female rats. Renal venous plasma norepinephrine levels after reperfusion were markedly elevated in male rats, but were not in female rats. These sex differences were eliminated by ovariectomy or treatment with tamoxifen, an estrogen receptor antagonist, in female rats. Furthermore, an intravenous injection of hexamethonium (25mg/kg), a ganglionic blocker, 5 min before ischemia suppressed the elevation in renal venous plasma norepinephrine levels after reperfusion, and attenuated renal dysfunction and histological damage in male rats, and ovariectomized and tamoxifen-treated female rats, but not in intact females. Thus, the present findings confirmed sex differences in the pathogenesis of ischemic acute kidney injury, and showed that the attenuation of ischemia/reperfusion-induced acute kidney injury observed in intact female rats may be dependent on depressing the renal sympathetic nervous system with endogenous estrogen.

  8. Expression of adenosine triphosphate-sensitive potassium channels in rats with cirrhosis: correlationship with sympathetic activity and renal function

    Directory of Open Access Journals (Sweden)

    Julio Cesar Martins Monte

    2006-12-01

    Full Text Available Objective: The aim of this study was to perform a direct analysis ofKATP mRNA expression by RT-PCR in kidney and isolated aorta fromrats with cirrhosis (induced by carbon tetrachloride and controls.The present study also analyses the relation between induced cirrhosisand urinary excretion of sodium and sympathetic activity in cirrhoticrats. Methods: Rats were placed in metabolic cages and allowedfree access to food and water. Cirrhosis was induced by repeateddoses of carbon tetrachloride by gastric gavage. After some weeks,the kidney and aorta were dissected and utilized for RNA extraction.Blood and urine were analyzed for electrolytes. Renal function wasestimated by creatinine clearance and sodium urinary excretion.Serum catecholamines were measured by HPLC analysis. Results:First, RT-PCR analysis showed that KATP mRNA is expressed in liverwith cirrhosis and intense fibrosis, but not with moderate fibrosis.Second, RT-PCR analysis revealed that KATP mRNA was detectedonly in aorta dissected from rats with cirrhosis. Finally, an enhancedreabsorption of sodium without renal failure suggests a potentialmediator would increase the activity of the sympathetic system.Conclusion: These results suggest that KATP mRNA is expressed incirrhotic rats with sympathetic activation and renal dysfunction. Thischannel might be involved in another route where the vascular tonecan be modulated in cirrhosis.

  9. Lack of uptake, release and action of UTP at sympathetic perivascular nerve terminals in rabbit ear artery.

    Science.gov (United States)

    Saïag, B; Shacoori, V; Bodin, P; Catheline, M; Burnstock, G

    1998-10-02

    A possible role of uridine 5'-triphosphate (UTP) and uridine at sympathetic nerve terminals was studied in the rabbit ear artery after incubation of isolated vessels with [3H]uridine or [3H]noradrenaline. It was found that [3H]uridine was taken up by rabbit ear artery. This uptake was largely suppressed after the removal of endothelium and was inhibited by ethidium bromide and dipyridamole. Chemical denervation of the vessels with 6-hydroxydopamine did not reduce the uptake. Following pre-incubation of the isolated vessels with [3H]uridine, there was a release of radioactivity from the superfused rabbit ear artery. UTP, UDP, UMP and uridine were detected by thin layer chromatography both in the superfusate and inside the vessels. Transmural electric stimulation (30 V, 5 Hz) induced a contraction of the vessels but did not increase the release of uridine nucleotides into the superfusate. [3H]Noradrenaline was released during electric stimulation and the addition of UTP (100 microM) had no effects on this release. To conclude, this study shows that in contrast to endothelial cells, the sympathetic nerve terminals of the rabbit ear artery do not take up uridine and do not release uridine-derived nucleotides. UTP at 100 microM is also unable to modulate the evoked release of noradrenaline. These results mainly confine the role of UTP in endothelium-derived vasodilatation via P2Y2 and/or P2Y4 receptors.

  10. Effects of three days of dry immersion on muscle sympathetic nerve activity and arterial blood pressure in humans.

    Science.gov (United States)

    Iwase, S; Sugiyama, Y; Miwa, C; Kamiya, A; Mano, T; Ohira, Y; Shenkman, B; Egorov, A I; Kozlovskaya, I B

    2000-03-15

    The present study was performed to determine how sympathetic function is altered by simulated microgravity, dry immersion for 3 days, and to elucidate the mechanism of post-spaceflight orthostatic intolerance in humans. Six healthy men aged 21-36 years old participated in the study. Before and after the dry immersion, subjects performed head-up tilt (HUT) test to 30 degrees and 60 degrees (5 min each) with recordings of muscle sympathetic nerve activity (MSNA, by microneurography), electrocardiogram, and arterial blood pressure (Finapres). Resting MSNA was increased after dry immersion from 23.7+/-3.2 to 40.9+/-3.0 bursts/min (p<0.005) without significant changes in resting heart rate (HR). MSNA responsiveness to orthostasis showed no significant difference but HR response was significantly augmented after dry immersion (p<0. 005). A significant diastolic blood pressure fall at 5th min of 60 degrees HUT was observed in five orthostatic tolerant subjects despite enough MSNA discharge after dry immersion. A subject suffered from presyncope at 2 min after 60 degrees HUT. He showed gradual blood pressure fall 10 s after 60 degrees HUT with initially well-maintained MSNA response and then with a gradually attenuated MSNA, followed by a sudden MSNA withdrawal and abrupt blood pressure drop. In conclusion, dry immersion increased MSNA without changing MSNA response to orthostasis, and resting HR, while increasing the HR response to orthostasis. Analyses of MSNA and blood pressure changes in orthostatic tolerant subjects and a subject with presyncope suggested that not only insufficient vasoconstriction to sympathetic stimuli, but also a central mechanism to induce a sympathetic withdrawal might play a role in the development of orthostatic intolerance after microgravity exposure.

  11. Hemodynamic and neural responses to renal denervation of the nerve to the clipped kidney by cryoablation in two-kidney, one-clip hypertensive rats.

    Science.gov (United States)

    Rossi, Noreen F; Pajewski, Russell; Chen, Haiping; Littrup, Peter J; Maliszewska-Scislo, Maria

    2016-01-15

    Renal artery stenosis is increasing in prevalence. Angioplasty plus stenting has not proven to be better than medical management. There has been a reluctance to use available denervation methodologies in this condition. We studied conscious, chronically instrumented, two-kidney, one-clip (2K-1C) Goldblatt rats, a model of renovascular hypertension, to test the hypothesis that renal denervation by cryoablation (cryo-DNX) of the renal nerve to the clipped kidney decreases mean arterial pressure (MAP), plasma and tissue ANG II, and contralateral renal sympathetic nerve activity (RSNA). Five-week-old male Sprague-Dawley rats underwent sham (ShC) or right renal artery clipping (2K-1C), placement of telemetry transmitters, and pair-feeding with a 0.4% NaCl diet. After 6 wk, rats were randomly assigned to cryo-DNX or sham cryotreatment (sham DNX) of the renal nerve to the clipped kidney. MAP was elevated in 2K-1C and decreased significantly in both ShC cryo-DNX and 2K-1C cryo-DNX. Tissue norepinephrine was ∼85% lower in cryo-DNX kidneys. Plasma ANG II was higher in 2K-1C sham DNX but not in 2K-1C cryo-DNX vs ShC. Renal tissue ANG II in the clipped kidney decreased after cryo-DNX. Baseline integrated RSNA of the unclipped kidney was threefold higher in 2K-1C versus ShC and decreased in 2K-1C cryo-DNX to values similar to ShC. Maximum reflex response of RSNA to baroreceptor unloading in 2K-1C was lower after cryo-DNX. Thus, denervation by cryoablation of the renal nerve to the clipped kidney decreases not only MAP but also plasma and renal tissue ANG II levels and RSNA to the contralateral kidney in conscious, freely moving 2K-1C rats.

  12. Effects of renal sympathetic denervation on 24-hour blood pressure variability

    Directory of Open Access Journals (Sweden)

    Christine Stefanie Zuern

    2012-05-01

    Full Text Available Background: In patients with arterial hypertension, increased blood pressure (BP variability contributes to end organ damage independently from mean levels of arterial BP. Increased BP variability has been linked to alterations in autonomic function including sympathetic overdrive. We hypothesized that catheter-based renal sympathetic denervation (RDN confers beneficial effects on BPV. Methods and Results: Eleven consecutive patients with therapy-refractory arterial hypertension (age 68.9±7.0 years; baseline systolic BP 189±23mmHg despite medication with 5.6±2.1 antihypertensive drugs underwent bilateral RDN. Twenty-four hour ambulatory blood pressure monitoring (ABPM was performed before RDN and six months thereafter. BPV was primarily assessed by means of standard deviation of 24-hour systolic arterial blood pressures (SDsys. Secondary measures of BPV were maximum systolic blood pressure (MAXsys and maximum difference between two consecutive readings of systolic BP (deltamaxsys over 24 hours. Six months after RDN, SDsys, MAXsys and deltamaxsys were significantly reduced from 16.9±4.6mmHg to 13.5±2.5mmHg (p=0.003, from 190±22mmHg to 172±20mmHg (p<0.001 and from 40±15mmHg to 28±7mmHg (p=0.006, respectively, without changes in concomitant antihypertensive therapy. Reductions of SDsys, MAXsys and deltamaxsys were observed in 10/11 (90.9%, 11/11 (100% and 9/11 (81.8% patients, respectively. Although we noted a significant reduction of systolic office blood pressure by 30.4±27.7mmHg (p=0.007, there was only a trend in reduction of average systolic BP assessed from ABPM (149±19mmHg to 142±18mmHg; p=0.086.Conclusions: In patients with therapy-refractory arterial hypertension, RDN leads to significant reductions of BP variability. Effects of RDN on BPV over 24 hours were more pronounced than on average levels of BP.

  13. Endothelial dysfunction and increased responses to renal nerve stimulation in rat kidneys during rhabdomyolysis-induced acute renal failure: role of hydroxyl radical.

    Science.gov (United States)

    Cil, Onur; Ertunc, Mert; Gucer, Kadri Safak; Ozaltin, Fatih; Iskit, Alper Bektas; Onur, Rustu

    2012-01-01

    Rhabdomyolysis is an important cause of acute renal failure (ARF) and renal vasoconstriction is the main mechanism in the pathogenesis of ARF. Lipid peroxidation due to hydroxyl radical (.OH) formation and redox cycling of myoglobin also have a role. We investigated the disturbance in renal vascular reactivity to reveal the mechanisms leading to ARF. Female Wistar rats (n = 7) were injected with glycerol (10 mL/kg, 50% in saline) intramuscularly to induce rhabdomyolysis, and then the kidneys were isolated and perfused. We investigated acetylcholine (ACh)-induced endothelium-dependent and papaverine (PAP)-induced endothelium-independent vasodilation responses and renal nerve stimulation (RNS)-induced vasoconstrictions. These were also investigated both in rats which received either .OH scavenger, dimethylthiourea (DMTU: 500 mg/kg before glycerol injection and 125 mg/kg 8 h after glycerol injection, n = 7), or myoglobin redox cycling inhibitor, acetaminophen (ApAP: 100 mg/kg 2 h before glycerol injection and 100 mg/kg each 4 h, and 22 h after glycerol injection, n = 7). ACh-induced responses in glycerol group were decreased (p group. DMTU restored both endothelium-dependent vasodilation and RNS-induced vasoconstriction. ApAP had no effect on vascular responses. Both DMTU and ApAP exerted a partial protective effect in renal histology without restoring serum creatinine and blood urea nitrogen (BUN) levels or creatinine clearance. This study showed that endothelial dysfunction and increased vasoconstriction developed during rhabdomyolysis. .OH plays an important role in the development of these vascular responses. These findings suggest that decreased endothelium-dependent vasodilation and augmented renal sympathetic tonus contribute to the development of renal vasoconstriction during rhabdomyolysis-induced ARF.

  14. Heart failure causes cholinergic transdifferentiation of cardiac sympathetic nerves via gp130-signaling cytokines in rodents.

    Science.gov (United States)

    Kanazawa, Hideaki; Ieda, Masaki; Kimura, Kensuke; Arai, Takahide; Kawaguchi-Manabe, Haruko; Matsuhashi, Tomohiro; Endo, Jin; Sano, Motoaki; Kawakami, Takashi; Kimura, Tokuhiro; Monkawa, Toshiaki; Hayashi, Matsuhiko; Iwanami, Akio; Okano, Hideyuki; Okada, Yasunori; Ishibashi-Ueda, Hatsue; Ogawa, Satoshi; Fukuda, Keiichi

    2010-02-01

    Although several cytokines and neurotrophic factors induce sympathetic neurons to transdifferentiate into cholinergic neurons in vitro, the physiological and pathophysiological roles of this remain unknown. During congestive heart failure (CHF), sympathetic neural tone is upregulated, but there is a paradoxical reduction in norepinephrine synthesis and reuptake in the cardiac sympathetic nervous system (SNS). Here we examined whether cholinergic transdifferentiation can occur in the cardiac SNS in rodent models of CHF and investigated the underlying molecular mechanism(s) using genetically modified mice. We used Dahl salt-sensitive rats to model CHF and found that, upon CHF induction, the cardiac SNS clearly acquired cholinergic characteristics. Of the various cholinergic differentiation factors, leukemia inhibitory factor (LIF) and cardiotrophin-1 were strongly upregulated in the ventricles of rats with CHF. Further, LIF and cardiotrophin-1 secreted from cultured failing rat cardiomyocytes induced cholinergic transdifferentiation in cultured sympathetic neurons, and this process was reversed by siRNAs targeting Lif and cardiotrophin-1. Consistent with the data in rats, heart-specific overexpression of LIF in mice caused cholinergic transdifferentiation in the cardiac SNS. Further, SNS-specific targeting of the gene encoding the gp130 subunit of the receptor for LIF and cardiotrophin-1 in mice prevented CHF-induced cholinergic transdifferentiation. Cholinergic transdifferentiation was also observed in the cardiac SNS of autopsied patients with CHF. Thus, CHF causes target-dependent cholinergic transdifferentiation of the cardiac SNS via gp130-signaling cytokines secreted from the failing myocardium.

  15. Responses of muscle spindles in feline dorsal neck muscles to electrical stimulation of the cervical sympathetic nerve.

    Science.gov (United States)

    Hellström, F; Roatta, S; Thunberg, J; Passatore, M; Djupsjöbacka, M

    2005-09-01

    Previous studies performed in jaw muscles of rabbits and rats have demonstrated that sympathetic outflow may affect the activity of muscle spindle afferents (MSAs). The resulting impairment of MSA information has been suggested to be involved in the genesis and spread of chronic muscle pain. The present study was designed to investigate sympathetic influences on muscle spindles in feline trapezius and splenius muscles (TrSp), as these muscles are commonly affected by chronic pain in humans. Experiments were carried out in cats anesthetized with alpha-chloralose. The effect of electrical stimulation (10 Hz for 90 s or 3 Hz for 5 min) of the peripheral stump of the cervical sympathetic nerve (CSN) was investigated on the discharge of TrSp MSAs (units classified as Ia-like and II-like) and on their responses to sinusoidal stretching of these muscles. In some of the experiments, the local microcirculation of the muscles was monitored by laser Doppler flowmetry. In total, 46 MSAs were recorded. Stimulation of the CSN at 10 Hz powerfully depressed the mean discharge rate of the majority of the tested MSAs (73%) and also affected the sensitivity of MSAs to sinusoidal changes of muscle length, which were evaluated in terms of amplitude and phase of the sinusoidal fitting of unitary activity. The amplitude was significantly reduced in Ia-like units and variably affected in II-like units, while in general the phase was affected little and not changed significantly in either group. The discharge of a smaller percentage of tested units was also modulated by 3-Hz CSN stimulation. Blockade of the neuromuscular junctions by pancuronium did not induce any changes in MSA responses to CSN stimulation, showing that these responses were not secondary to changes in extrafusal or fusimotor activity. Further data showed that the sympathetically induced modulation of MSA discharge was not secondary to the concomitant reduction of muscle blood flow induced by the stimulation. Hence

  16. Renal sympathetic denervation prevents the development of pulmonary arterial hypertension and cardiac dysfunction in dogs

    Directory of Open Access Journals (Sweden)

    Wei Hu

    2015-08-01

    Full Text Available The renin–angiotensin–aldosterone system is activated in pulmonary arterial hypertension (PAH patients, and this activation may have long-term negative effects on the progression of PAH. The purpose of this study was to evaluate the effects of transcatheter renal sympathetic denervation (RSD on the development of pulmonary arterial hypertension and cardiac dysfunction in dogs using two-dimensional speckle tracking imaging. Twenty-two dogs were randomly divided into three groups: control group (n = 7, PAH group (n = 8, and PAH + RSD group (n = 7. All dogs were assessed using two-dimensional speckle tracking imaging. The ventricular strain, ventricular synchrony, left ventricular (LV twist, and torsion rate were analyzed to evaluate cardiac function. After 8 weeks, the right ventricular lateral longitudinal strain and the septum longitudinal strain were reduced in the PAH group compared with the control group (p < 0.001. However, these values were significantly restored in the PAH + RSD group compared with the PAH group (p < 0.01. The degree of LV and RV dyssynchrony was significantly higher in the PAH group compared with the control group (p < 0.001, but the degree of LV and RV dyssynchrony was significantly lower in the PAH + RSD group compared to the PAH group (p < 0.01. The LV twist was significantly restored in the PAH + RSD group compared to the PAH group (p < 0.01. Similarly, the rotation rate was markedly decreased in the PAH group, and strikingly improved in the PAH + RSD group (p < 0.01. These results indicate that RSD prevents the development of PAH and cardiac dysfunction in dogs.

  17. Muscle Sympathetic Nerve Activity During Intense Lower Body Negative Pressure to Presyncope in Humans

    Science.gov (United States)

    2009-08-24

    Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, 1996). As diastolic arterial pressure... dogs . Am J Physiol Heart Circ Physiol 274, H1099–H1105. Preiss G & Polosa C (1974). Patterns of sympathetic neuron activity associated with Mayer waves...Society of Cardiology and the North American Society of Pacing and Electrophysiology (1996). Heart rate variability: standards of measurement

  18. Sex Comparisons in Muscle Sympathetic Nerve Activity and Arterial Pressure Oscillations During Progressive Central Hypovolemia

    Science.gov (United States)

    2015-01-01

    sympathetic activity in humans. Am. J. Physiol. 287:H1658–H1662. Convertino, V. A. 1996. Clinical aspects of the control of plasma volume at microgravity and...standards of measurement, physiological interpretation, and clinical use. Circulation 93:1043–1065. Ichinose, M., M. Saito, A. Kitano, K. Hayashi, N...G. Huang, S. A. Smith, R. Zhang, and K. J. Formes. 2003. Aging and arterial blood pressure variability during orthostatic challenge. Gerontology 49

  19. Heart rate modulation by sympathetic nerves in dogs with heart failure.

    Science.gov (United States)

    Uechi, Masami; Shimizu, Akira; Mizuno, Masashi

    2002-11-01

    To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (control dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma catecholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure.

  20. Renal Sympathetic Denervation by CT-Guided Ethanol Injection: A Phase II Pilot Trial of a Novel Technique

    Energy Technology Data Exchange (ETDEWEB)

    Ricke, J., E-mail: jens.ricke@med.ovgu.de; Seidensticker, M.; Becker, S. [Otto-von-Guericke University Magdeburg, Department of Radiology and Nuclear Medicine, Universitätsklinikum Magdeburg AöR (Germany); Schiefer, J. [Universitätsklinikum Magdeburg AöR, Department of Nephrology and Hypertension, Diabetes and Endocrinology (Germany); Adamchic, I.; Lohfink, K. [Otto-von-Guericke University Magdeburg, Department of Radiology and Nuclear Medicine, Universitätsklinikum Magdeburg AöR (Germany); Kandulski, M.; Heller, A.; Mertens, P. R. [Universitätsklinikum Magdeburg AöR, Department of Nephrology and Hypertension, Diabetes and Endocrinology (Germany)

    2016-02-15

    ObjectivesCT-guided ethanol-mediated renal sympathetic denervation in treatment of therapy-resistant hypertension was performed to assess patient safety and collect preliminary data on treatment efficacy.Materials and MethodsEleven patients with therapy-resistant hypertension (blood pressure of >160 mmHg despite three different antihypertensive drugs including a diuretic) and following screening for secondary causes were enrolled in a phase II single arm open label pilot trial of CT-guided neurolysis of sympathetic renal innervation. Primary endpoint was safety, and secondary endpoint was a decrease of the mean office as well as 24-h systolic blood pressure in follow-up. Follow-up visits at 4 weeks, 3, and 6 months included 24-h blood pressure assessments, office blood pressure, laboratory values, as well as full clinical and quality of life assessments.ResultsNo toxicities ≥3° occurred. Three patients exhibited worsened kidney function in follow-up analyses. When accounting all patients, office systolic blood pressure decreased significantly at all follow-up visits (maximal mean decrease −41.2 mmHg at 3 months). The mean 24-h systolic blood pressure values decreased significantly at 3 months, but not at 6 months (mean: −9.7 and −6.3 mmHg, respectively). Exclusion of five patients who had failed catheter-based endovascular denervation and/or were incompliant for antihypertensive drug intake revealed a more pronounced decrease of 24-h systolic blood pressure (mean: −18.3 and −15.2 mmHg at 3 and 6 months, p = 0.03 and 0.06).ConclusionCT-guided sympathetic denervation proved to be safe and applicable under various anatomical conditions with more renal arteries and such of small diameter.

  1. Macrophage depletion lowers blood pressure and restores sympathetic nerve α2-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats

    Science.gov (United States)

    Thang, Loc V.; Demel, Stacie L.; Crawford, Robert; Kaminski, Norbert E.; Swain, Greg M.; Van Rooijen, Nico

    2015-01-01

    We tested the hypothesis that vascular macrophage infiltration and O2− release impairs sympathetic nerve α2-adrenergic autoreceptor (α2AR) function in mesenteric arteries (MAs) of DOCA-salt hypertensive rats. Male rats were uninephrectomized or sham operated (sham). DOCA pellets were implanted subcutaneously in uninephrectomized rats who were provided high-salt drinking water or high-salt water with apocynin. Sham rats received tap water. Blood pressure was measured using radiotelemetry. Treatment of sham and DOCA-salt rats with liposome-encapsulated clodronate was used to deplete macrophages. After 3–5, 10–13, and 18–21 days of DOCA-salt treatment, MAs and peritoneal fluid were harvested from euthanized rats. Norepinephrine (NE) release from periarterial sympathetic nerves was measured in vitro using amperometry with microelectrodes. Macrophage infiltration into MAs as well as TNF-α and p22phox were measured using immunohistochemistry. Peritoneal macrophage activation was measured by flow cytometry. O2− was measured using dihydroethidium staining. Hypertension developed over 28 days, and apocynin reduced blood pressure on days 18–21. O2− and macrophage infiltration were greater in DOCA-salt MAs compared with sham MAs after day 10. Peritoneal macrophage activation occurred after day 10 in DOCA-salt rats. Macrophages expressing TNF-α and p22phox were localized near sympathetic nerves. Impaired α2AR function and increased NE release from sympathetic nerves occurred in MAs from DOCA-salt rats after day 18. Macrophage depletion reduced blood pressure and vascular O2− while restoring α2AR function in DOCA-salt rats. Macrophage infiltration into the vascular adventitia contributes to increased blood pressure in DOCA-salt rats by releasing O2−, which disrupts α2AR function, causing enhanced NE release from sympathetic nerves. PMID:26320034

  2. Pituitary adenylyl cyclase-activating polypeptide and nerve growth factor use the proteasome to rescue nerve growth factor-deprived sympathetic neurons cultured from chick embryos.

    Science.gov (United States)

    Przywara, D A; Kulkarni, J S; Wakade, T D; Leontiev, D V; Wakade, A R

    1998-11-01

    Removal of nerve growth factor (NGF) from sympathetic neurons initiates a neuronal death program and apoptosis. We show that pituitary adenylyl cyclase-activating polypeptide (PACAP) prevents apoptosis in NGF-deprived sympathetic neurons. PACAP (100 nM) added to culture medium at the time of plating failed to support neuronal survival. However, in neurons grown for 2 days with NGF and then deprived of NGF, PACAP prevented cell death for the next 24-48 h. Uptake of [3H]norepinephrine ([3H]NE) was used as an index of survival and decreased >50% in NGF-deprived cultures within 24 h. PACAP (1-100 nM) restored [3H]NE uptake to 92 +/- 8% of that of NGF-supported controls. Depolarization-induced [3H]NE release in neurons rescued by PACAP was the same as that in NGF-supported neurons. PACAP rescue was not mimicked by forskolin or 8-bromo-cyclic AMP and was not blocked by the protein kinase A inhibitor Rp-adenosine 3',5'-cyclic monophosphothioate. Mobilization of phosphatidylinositol by muscarine failed to support NGF-deprived neurons. Thus, PACAP may use novel signaling to promote survival of sympathetic neurons. The apoptosis-associated caspase CPP32 activity increased approximately fourfold during 6 h of NGF withdrawal (145 +/- 40 versus 38 +/- 17 nmol of substrate cleaved/min/mg of protein) and returned to even below the control level in NGF-deprived, PACAP-rescued cultures (14 +/- 7 nmol/min/mg of protein). Readdition of NGF or PACAP to NGF-deprived cultures reversed CPP32 activation, and this was blocked by lactacystin, a potent and specific inhibitor of the 20S proteasome, suggesting that NGF and PACAP target CPP32 for destruction by the proteasome. As PACAP is a preganglionic neurotransmitter in autonomic ganglia, we propose a novel function for this transmitter as an apoptotic rescuer of sympathetic neurons when the supply of NGF is compromised.

  3. The role of sympathetic and parasympathetic nerve systems on the smooth muscle of rat seminal vesicles - experimental results and speculation for physiological implication on ejaculation.

    Science.gov (United States)

    Hsieh, J-T; Kuo, Y-C; Chang, H-C; Liu, S-P; Chen, J-H; Tsai, V F S

    2014-01-01

    Ejaculation is a process involving sympathetic and parasympathetic effects during different stages - emission and ejection. Some conditions of ejaculation dysfunction are associated with autonomic nerves. However, the exact effects of autonomic nerves on ejaculation are not well defined. Autonomic agonists induce different recorded trace patterns of seminal vesicular contraction. The different traces contain different components of phasic and tonic contraction, which may have physiological implications. In this study, we examined isolated rat seminal vesicle (SV) contraction by phenylephrine (PE), acetylcholine, and their respective antagonists and then speculated upon physiological roles of sympathetic and parasympathetic nerves on SV during ejaculation. We found that PE and Ach both achieved good contraction of rat SV. Compared to α1b for sympathetic and M1, M2 for parasympathetic receptors, α1a and M3 are the relatively dominant subtypes on rat SV. Adrenergic and cholinergic agonists cause different trace patterns of SV contraction. We speculated that the sympathetic effect is dominant during emission to squeeze seminal fluid out and that the parasympathetic effect is dominant during ejection to provide an anti-reflux effect on the ejaculatory duct.

  4. Plasma volume substitution does not inhibit plasma noradrenaline and muscle nerve sympathetic responses to insulin-induced hypoglycaemia in healthy humans

    DEFF Research Database (Denmark)

    Frandsen, Henrik Lund; Berne, C; Fagius, J;

    1989-01-01

    underly the sympathetic activation. To study the effect of prevention of plasma volume reduction during hypoglycaemia, saline containing albumin was infused intravenously in healthy adult volunteers during hypoglycaemia. Hypoglycaemia was induced by an intravenous injection of soluble insulin in a dose...... of 0.15 IU/kg body weight. Peripheral venous plasma noradrenaline concentrations were identical in experiments without and with plasma volume substitution. Muscle nerve sympathetic activity increased to the same extent during hypoglycaemia with and without plasma volume substitution. It is concluded...

  5. Effect of cortisol on muscle sympathetic nerve activity in Pima Indians and Caucasians.

    Science.gov (United States)

    Vozarova, Barbora; Weyer, Christian; Snitker, Soren; Gautier, Jean-Francois; Cizza, Giovanni; Chrousos, George; Ravussin, Eric; Tataranni, P Antonio

    2003-07-01

    The hypothalamo-pituitary-adrenal axis and sympathetic nervous system (SNS) interact to maintain cardiovascular and metabolic homeostasis, especially during stress. Pima Indians have a low SNS activity, which may contribute to both their increased risk of obesity and reduced risk of hypertension. Although glucocorticoids inhibit SNS activity, Pima Indians are not hypercortisolemic compared with Caucasians. This does not exclude the possibility that the SNS is more responsive to an inhibitory effect of cortisol in the former than in the latter group. We measured fasting plasma ACTH and cortisol and muscle SNS activity [muscle sympathetic nervous system activity (MSNA), microneurography] in 58 males [27 Pimas/31 Caucasians]. Seven Pimas and 12 Caucasians were randomized to a double-blind, placebo-controlled, cross-over study to examine the effect of overnight partial chemical adrenalectomy (metyrapone) followed by cortisol replacement (hydrocortisone) on plasma ACTH, cortisol, and MSNA. There were no ethnic differences in fasting plasma ACTH or cortisol, but MSNA adjusted for percent body fat was lower in Pimas than in Caucasians (P fasting cortisol and basal MSNA. Administration of metyrapone did not lead to significant changes in MSNA. In response to a hydrocortisone infusion, MSNA decreased in Pima Indians (P = 0.03) but not in Caucasians (P = 0.7). Our data indicate that the low SNS activity that predisposes Pima Indians to obesity is not due to a tonic inhibitory effect of cortisol. However, an acute release of cortisol is likely to more effectively contain sympathoexcitation during stress in Pima Indians than in Caucasians, which may be an important mechanism of cardioprotection in this Native American population.

  6. Usefulness of Cardiac Sympathetic Nerve Imaging Using (123)Iodine-Metaiodobenzylguanidine Scintigraphy for Predicting Sudden Cardiac Death in Patients With Heart Failure.

    Science.gov (United States)

    Kasama, Shu; Toyama, Takuji; Kurabayashi, Masahiko

    2016-01-01

    The autonomic nervous system plays an important role in the human heart. Activation of the cardiac sympathetic nervous system is a cardinal pathophysiological abnormality associated with the failing human heart. Myocardial imaging using (123)I-metaiodobenzylguanidine (MIBG), an analog of norepinephrine, can be used to investigate the activity of norepinephrine, the predominant neurotransmitter of the sympathetic nervous system. Many clinical trials have demonstrated that (123)I-MIBG scintigraphic parameters predict cardiac adverse events, especially sudden cardiac death, in patients with heart failure. In this review, we summarize results from published studies that have focused on the use of cardiac sympathetic nerve imaging using (123)I-MIBG scintigraphy for risk stratification of sudden cardiac death in patients with heart failure.

  7. Functional and structural changes in the brain associated with the increase in muscle sympathetic nerve activity in obstructive sleep apnoea

    Directory of Open Access Journals (Sweden)

    Rania H. Fatouleh

    2014-01-01

    Full Text Available Muscle sympathetic nerve activity (MSNA is greatly elevated in patients with obstructive sleep apnoea (OSA during daytime wakefulness, leading to hypertension, but the underlying mechanisms are poorly understood. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI of the brain we aimed to identify the central processes responsible for the sympathoexcitation. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted percutaneously into the common peroneal nerve in 17 OSA patients and 15 healthy controls lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes sampling protocol. Fluctuations in BOLD signal intensity covaried with the intensity of the concurrently recorded bursts of MSNA. In both groups there was a positive correlation between MSNA and signal intensity in the left and right insulae, dorsolateral prefrontal cortex (dlPFC, dorsal precuneus, sensorimotor cortex and posterior temporal cortex, and the right mid-cingulate cortex and hypothalamus. In OSA the left and right dlPFC, medial PFC (mPFC, dorsal precuneus, anterior cingulate cortex, retrosplenial cortex and caudate nucleus showed augmented signal changes compared with controls, while the right hippocampus/parahippocampus signal intensity decreased in controls but did not change in the OSA subjects. In addition, there were significant increases in grey matter volume in the left mid-insula, the right insula, left and right primary motor cortices, left premotor cortex, left hippocampus and within the brainstem and cerebellum, and significant decreases in the mPFC, occipital lobe, right posterior cingulate cortex, left cerebellar cortex and the left and right amygdala in OSA, but there was no overlap between these structural changes and the functional changes in OSA. These data suggest that the elevated muscle

  8. Effects of nicorandil on cardiac sympathetic nerve activity after reperfusion therapy in patients with first anterior acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Kasama, Shu; Toyama, Takuji; Suzuki, Tadashi; Kurabayashi, Masahiko [Gunma University School of Medicine, Department of Cardiovascular Medicine, Maebashi (Japan); Kumakura, Hisao; Takayama, Yoshiaki; Ichikawa, Shuichi [Cardiovascular Hospital of Central Japan, Gunma (Japan)

    2005-03-01

    Ischaemic preconditioning (PC) is a cardioprotective phenomenon in which short periods of myocardial ischaemia result in resistance to decreased contractile dysfunction during a subsequent period of sustained ischaemia. Nicorandil, an ATP-sensitive potassium channel opener, can induce PC effects on sympathetic nerves during myocardial ischaemia. However, its effects on cardiac sympathetic nerve activity (CSNA) and left ventricular remodelling have not been determined. In this study, we sought to determine whether nicorandil administration improves CSNA in patients with acute myocardial infarction (AMI). We studied 58 patients with first anterior AMI, who were randomly assigned to receive nicorandil (group A) or isosorbide dinitrate (group B) after primary coronary angioplasty. The nicorandil or isosorbide dinitrate was continuously infused for >48 h. The extent score (ES) was determined from {sup 99m}Tc-pyrophosphate scintigraphy, and the total defect score (TDS) was determined from {sup 201}Tl scintigraphy 3-5 days after primary angioplasty. The left ventricular end-diastolic volume (LVEDV) and left ventricular ejection fraction (LVEF) were determined by left ventriculography 2 weeks later. The delayed heart/mediastinum count (H/M) ratio, delayed TDS and washout rate (WR) were determined from {sup 123}I-meta-iodobenzylguanidine (MIBG) images 3 weeks later. The left ventriculography results were re-examined 6 months after treatment. Fifty patients originally enrolled in the trial completed the entire protocol. After treatment, no significant differences were observed in ES or left ventricular parameters between the two groups. However, in group A (n=25), the TDSs determined from {sup 201}Tl and {sup 123}I-MIBG were significantly lower (26{+-}6 vs 30{+-}5, P<0.01, and 32{+-}8 vs 40{+-}6, P<0.0001, respectively), the H/M ratio significantly higher (1.99{+-}0.16 vs 1.77{+-}0.30, P<0.005) and the WR significantly lower (36%{+-}8% vs 44%{+-}12%, P<0.005) than in group B

  9. Targeted NGF siRNA delivery attenuates sympathetic nerve sprouting and deteriorates cardiac dysfunction in rats with myocardial infarction.

    Directory of Open Access Journals (Sweden)

    Hesheng Hu

    Full Text Available Nerve growth factor (NGF is involved in nerve sprouting, hyper-innervation, angiogenesis, anti-apoptosis, and preservation of cardiac function after myocardial infarction (MI. Positively modulating NGF expression may represent a novel pharmacological strategy to improve post-infarction prognosis. In this study, lentivirus encoding NGF short interfering RNA (siRNA was prepared, and MI was modeled in the rat using left anterior descending coronary artery ligation. Rats were randomly grouped to receive intramyocardial injection of lentiviral solution containing NGF-siRNA (n = 19, MI-SiNGF group, lentiviral solution containing empty vector (n = 18, MI-GFP group or 0.9% NaCl solution (n = 18, MI-control group, or to receive thoracotomy and pericardiotomy (n = 17, sham-operated group. At 1, 2, 4, and 8 wk after transduction, rats in the MI-control group had higher levels of NGF mRNA and protein than those in the sham-operated group, rats in the MI-GFP group showed similar levels as the MI-control group, and rats in the MI-SiNGF group had lower levels compared to the MI-GFP group, indicating that MI model was successfully established and NGF siRNA effectively inhibited the expression of NGF. At 8 wk, echocardiographic and hemodynamic studies revealed a more severe cardiac dysfunction in the MI-siRNA group compared to the MI-GFP group. Moreover, rats in the MI-siRNA group had lower mRNA and protein expression levels of tyrosine hydroxylase (TH and growth-associated protein 43-positive nerve fibers (GAP-43 at both the infarcted border and within the non-infarcted left ventricles (LV. NGF silencing also reduced the vascular endothelial growth factor (VEGF expression and decreased the arteriolar and capillary densities at the infarcted border compared to the MI-GFP group. Histological analysis indicated a large infarcted size in the MI-SiNGF group. These findings suggested that endogenous NGF silencing attenuated sympathetic nerve sprouting

  10. Evaluation of sympathetic nerve system activity with MIBG. Comparison with heart rate variability

    Energy Technology Data Exchange (ETDEWEB)

    Kurata, Chinori; Wakabayashi, Yasushi; Shouda, Sakae; Mikami, Tadashi [Hamamatsu Medical School (Japan); Tawarahara, Kei; Sugiyama, Tsuyoshi; Nakano, Tomoyasu; Suzuki, Toshihiko

    1997-04-01

    Authors attempted to elucidate the relations of plasma concentration of norepinephrine (pNE) and findings of heart rate variability and MIBG myocardial scintigraphy and evaluated cardiac autonomic nervous activity in chronic renal failure. Subjects were 211 patients with various heart diseases (coronary artery lesion, cardiomyopathy, hypertension, diabetes mellitus, renal failure and so on), 60 patients with artificial kidney due to chronic renal failure, 13 of whom were found to have coronary arterial disease by Tl myocardial scintigraphy, and 14 normal volunteers. ECG was recorded with the portable recorder for heart rate variability. Together with collection of blood for pNE measurement, myocardial scintigraphy was done at 15 and 150 min after intravenous administration of 111 MBq of MIBG for acquisition of early and delayed, respectively, images of the frontal breast. Accumulation at and elimination during the time points of MIBG were computed in cps unit. Variability of heart rate was found to have the correlation positive with MIBG delayed accumulation and negative with the elimination, and pNE, negative with heart rate variability and the delayed accumulation and positive with the elimination. Thus cardiac autonomic nervous abnormality was suggested to occur before uremic cardiomyopathy. (K.H.)

  11. Effects of Spinal Cord Stimulation on Cardiac Sympathetic Nerve Activity in Patients with Heart Failure

    DEFF Research Database (Denmark)

    Naar, Jan; Jaye, Deborah; Linde, Cecilia

    2017-01-01

    activity in HF patients. Secondary hypotheses were that SCS improves left ventricular function and dimension, exercise capacity, and clinical variables relevant to HF. METHODS: HF patients with a SCS device previously participating in the DEFEAT-HF trial were included in this crossover study with 6-week...... intervention periods (SCS-ON and SCS-OFF). SCS (50 Hz, 210-μs pulse duration, aiming at T2-T4 segments) was delivered for 12 hours daily. Indices of myocardial sympathetic neuronal function (heart-to-mediastinum ratio, HMR) and activity (washout rate, WR) were assessed using (123) I......-metaiodobenzylguanidine (MIBG) scintigraphy. Echocardiography, exercise testing, and clinical data collection were also performed. RESULTS: We included 13 patients (65.3 ± 8.0 years, nine males) and MIBG scintigraphy data were available in 10. HMR was not different comparing SCS-ON (1.37 ± 0.16) and SCS-OFF (1.41 ± 0.21, P = 0...

  12. CT-clinical approach to patients with symptoms related to the V, VII, IX-XII cranial nerves and cervical sympathetics

    Energy Technology Data Exchange (ETDEWEB)

    Kalovidouris, A.; Mancuso, A.A.; Dillon, W.

    1984-06-01

    Forty-three patients who had signs and symptoms possibly related to the extracranial course of cranial nerves V, VII, IX, X-XII, and the cervical sympathetics were examined prospectively using high resolution CT to obtain images of thin sections during rapid drip infusion of contrast material. Anatomic areas in the scan protocols included the posterior fossa, cavernous and paranasal sinuses, skull base, temporal bone, nasopharynx, parotid gland, tongue base, and neck. Nine of the 23 patients with possible fifth nerve deficits had extracranial structural lesions that explained the symptoms; none of these nine, however, had typical trigeminal neuralgia. Of eight patients with peripheral seventh nerve abnormalities, two had positive findings on scans. Of five patients presenting with referred ear pain, three had carcinoma of the upper aerodigestive tract. The authors' experience suggests that patients at high risk for structural lesions responsible for cranial nerve deficits can be selected by clinical criteria. Protocols for each clinical setting are presented.

  13. [A pharmacological analysis of the central control of the preganglionic sympathetic neurons during stimulation of the afferent nerve fibers of the digestive tract].

    Science.gov (United States)

    Itina, L V; Posniak, V A

    1995-12-01

    In acute experiments on cats, effect of adrenergic brain neurons on impulse activity of preganglionic fibers of the left splanchnic nerve was studied. Afferent fibers of nerves innervating the stomach, duodenum, ileum and ileocecal angle were electrically stimulated. Phenoxybenzamine, obsidan, amizyl, iprazid, nuredal, dalargine, and morphine were used for pharmacological analysis. Nerves, stimulation at 20 Hz of different segments of the digestive tract was accompanied by different inhibition of preganglionic neurons. Sympathetic-stimulating effects were observed more frequently at 5 Hz stimulation. After vagotomy, alpha- and beta-adrenoreceptor block, central cholinoreceptor and monoamine oxidase (MAO) block, and after dalargine (0.1 and 0.01 mg/kg) nerves stimulation at 20 Hz was followed by sympathetic-stimulating effect. A weak regulatory effect of morphine (1 and 10 mg/kg) on ileal nerve stimulation effects was shown. It is suggested that excitation from afferent neurons of the vagus is transmitted to central cholinergic neurons which, in their turn, excite adrenergic neurons of the brain, and the latter inhibit impulsation of preganglionic fibers. MAO block increased the balance of excitatory effect of serotonin on spinal reflexes. Morphine and dalargine intracentrally may block adrenergic and cholinergic transmissions, as well as decrease the release of substance P from afferent neurons. Their regulatory action is revealed when different frequencies of stimulation are used.

  14. Inhibition of noradrenaline release from the sympathetic nerves of the human saphenous vein by presynaptic histamine H3 receptors.

    Science.gov (United States)

    Molderings, G J; Weissenborn, G; Schlicker, E; Likungu, J; Göthert, M

    1992-07-01

    The human saphenous vein was used to examine whether presynaptic histamine receptors can modulate noradrenaline release and, if so, to determine their pharmacological characteristics. Strips of this blood vessel were incubated with [3H]noradrenaline and subsequently superfused with physiological salt solution containing desipramine and corticosterone. Electrically (2 Hz) evoked 3H overflow was inhibited by histamine and the H3 receptor agonist R-(-)-alpha-methylhistamine. Histamine-induced inhibition of electrically evoked tritium overflow was not affected by alpha 2-adrenoceptor blockade by rauwolscine. S-(+)-alpha-methylhistamine (up to 10 mumol/l) as well as the histamine H1 and H2 receptor agonists 2-(2-thiazolyl)ethylamine (up to 3 mumol/l) and dimaprit (up to 30 mumol/l), respectively, were ineffective. The selective histamine H3 receptor antagonist thioperamide abolished the inhibitory effect of histamine. The histamine H2 and H1 receptor antagonists ranitidine and pheniramine, respectively, did not affect the histamine-induced inhibition of evoked tritium overflow. The present results are compatible with the suggestion that the sympathetic nerves of the human saphenous vein are endowed with inhibitory presynaptic histamine receptors of the H3 class.

  15. Effects of inhaled citronella oil and related compounds on rat body weight and brown adipose tissue sympathetic nerve.

    Science.gov (United States)

    Batubara, Irmanida; Suparto, Irma H; Sa'diah, Siti; Matsuoka, Ryunosuke; Mitsunaga, Tohru

    2015-03-12

    Citronella oil is one of the most famous Indonesian essential oils, having a distinctive aroma. As with other essential oils, it is crucial to explore the effects of inhalation of this oil. Therefore, the aim of this research was to elucidate the effects of inhalation of citronella oil and its components isolated from Cymbopogon nardus L. (Poaceae), Indonesian local name: "Sereh Wangi" on the body weight, blood lipid profile, and liver function of rats, as well as on the sympathetic nerve activity and temperature of brown adipose tissue. Sprague-Dawley male adult rats fed with high fat diet (HFD) were made to inhale citronella oil, R-(+)-citronellal, and β-citronellol for five weeks, and the observations were compared to those of HFD rats that were not subjected to inhalation treatment. The results showed that inhalation of β-citronellol decreased feed consumption. As a consequence, the percentage of weight gain decreased compared with that in control group and the blood cholesterol level in the β-citronellol group was significantly lowered. Concentration of liver function enzymes were not significantly different among the groups. In conclusion, inhalation of citronella oil, specifically β-citronellol, decreased body weight by decreasing appetite, without any marked changes in liver enzyme concentrations.

  16. Effects of Inhaled Citronella Oil and Related Compounds on Rat Body Weight and Brown Adipose Tissue Sympathetic Nerve

    Directory of Open Access Journals (Sweden)

    Irmanida Batubara

    2015-03-01

    Full Text Available Citronella oil is one of the most famous Indonesian essential oils, having a distinctive aroma. As with other essential oils, it is crucial to explore the effects of inhalation of this oil. Therefore, the aim of this research was to elucidate the effects of inhalation of citronella oil and its components isolated from Cymbopogon nardus L. (Poaceae, Indonesian local name: “Sereh Wangi” on the body weight, blood lipid profile, and liver function of rats, as well as on the sympathetic nerve activity and temperature of brown adipose tissue. Sprague-Dawley male adult rats fed with high fat diet (HFD were made to inhale citronella oil, R-(+-citronellal, and β-citronellol for five weeks, and the observations were compared to those of HFD rats that were not subjected to inhalation treatment. The results showed that inhalation of β-citronellol decreased feed consumption. As a consequence, the percentage of weight gain decreased compared with that in control group and the blood cholesterol level in the β-citronellol group was significantly lowered. Concentration of liver function enzymes were not significantly different among the groups. In conclusion, inhalation of citronella oil, specifically β-citronellol, decreased body weight by decreasing appetite, without any marked changes in liver enzyme concentrations.

  17. Impact of gender on benefits of exercise training on sympathetic nerve activity and muscle blood flow in heart failure.

    Science.gov (United States)

    Antunes-Correa, Ligia M; Melo, Ruth C; Nobre, Thais S; Ueno, Linda M; Franco, Fabio G M; Braga, Ana M W; Rondon, Maria U P B; Brum, Patricia C; Barretto, Antonio C P; Middlekauff, Holly R; Negrao, Carlos E

    2010-01-01

    We compared the effects of exercise training on neurovascular control and functional capacity in men and women with chronic heart failure (HF). Forty consecutive HF outpatients from the Heart Institute, University of Sao Paulo, Brazil were divided into the following four groups matched by age: men exercise-trained (n = 12), men untrained (n = 10), women exercise-trained (n = 9), women untrained (n = 9). Maximal exercise capacity was determined from a maximal progressive exercise test on a cycle ergometer. Forearm blood flow was measured by venous occlusion plethysmography. Muscle sympathetic nerve activity (MSNA) was recorded directly using the technique of microneurography. There were no differences between groups in any baseline parameters. Exercise training produced a similar reduction in resting MSNA (P = 0.000002) and forearm vascular resistance (P = 0.0003), in men and women with HF. Peak VO(2) was similarly increased in men and women with HF (P = 0.0003) and VE/VCO(2) slope was significantly decreased in men and women with HF (P = 0.0007). There were no significant changes in left-ventricular ejection fraction in men and women with HF. The benefits of exercise training on neurovascular control and functional capacity in patients with HF are independent of gender.

  18. Fluorescence histochemistry and autoradiography of adrenergic nerves in the renal juxtaglomerular complex of mammals and man, with special regard to the efferent arteriole.

    Science.gov (United States)

    Dolezel, S; Edvinsson, L; Owman, C; Owman, T

    1976-06-14

    The adrenergic innervation of the juxtaglomerular complex was studied in kidneys from mice, rats, guinea-pigs, rabbits, cats, dogs, pigs, monkeys, and humans using fluorescence histochemistry of neuronal noradrenaline and autoradiography of 3H-noradrenaline. The localization of the nerves was established by phase contrast optics or by perfusing the vascular system with India ink. Adrenergic nerve terminals, exhibiting a formaldehyde-induced fluorescence and having the ability to take up and accumulate 3H-noradrenaline, were easily identified when they enclosed the glomerular afferent arteriole. They continued in between and close to the macula densa and lacis cells to supply the glomerular efferent arteriole. The nerves could be seen to accompany this arteriole for a considerable distance until they branched off to the vasa recta in the juxtamedullary region and to adjacent cortical veins. This innervation pattern was found to be a constant feature except in kidneys from guinea-pigs and cats, in which post-glomerular units. The fluorescence in all adrenergic fibres supplying the juxtaglomerular complex disappeared after removal of the aortico-renal ganglion, showing that they belong to a common system of renal sympathetic nerves.

  19. Roles of estrogen and progesterone in modulating renal nerve function in the rat kidney

    Directory of Open Access Journals (Sweden)

    J.B. Graceli

    2013-07-01

    Full Text Available The maintenance of extracellular Na+ and Cl- concentrations in mammals depends, at least in part, on renal function. It has been shown that neural and endocrine mechanisms regulate extracellular fluid volume and transport of electrolytes along nephrons. Studies of sex hormones and renal nerves suggested that sex hormones modulate renal function, although this relationship is not well understood in the kidney. To better understand the role of these hormones on the effects that renal nerves have on Na+ and Cl- reabsorption, we studied the effects of renal denervation and oophorectomy in female rats. Oophorectomized (OVX rats received 17β-estradiol benzoate (OVE, 2.0 mg·kg-1·day-1, sc and progesterone (OVP, 1.7 mg·kg-1·day-1, sc. We assessed Na+ and Cl- fractional excretion (FENa+ and FECl- , respectively and renal and plasma catecholamine release concentrations. FENa+ , FECl- , water intake, urinary flow, and renal and plasma catecholamine release levels increased in OVX vs control rats. These effects were reversed by 17β-estradiol benzoate but not by progesterone. Renal denervation did not alter FENa+ , FECl- , water intake, or urinary flow values vs controls. However, the renal catecholamine release level was decreased in the OVP (236.6±36.1 ng/g and denervated rat groups (D: 102.1±15.7; ODE: 108.7±23.2; ODP: 101.1±22.1 ng/g. Furthermore, combining OVX + D (OD: 111.9±25.4 decreased renal catecholamine release levels compared to either treatment alone. OVE normalized and OVP reduced renal catecholamine release levels, and the effects on plasma catecholamine release levels were reversed by ODE and ODP replacement in OD. These data suggest that progesterone may influence catecholamine release levels by renal innervation and that there are complex interactions among renal nerves, estrogen, and progesterone in the modulation of renal function.

  20. Renal denervation in chronic kidney disease

    NARCIS (Netherlands)

    Blankestijn, Peter J.; Joles, Jaap A.

    2012-01-01

    Previous studies have indicated that ablation of renal sympathetic nerves reduces blood pressure in patients with resistant hypertension and preserved renal function. Hering et al. have now investigated the efficacy and safety of this procedure in patients with moderate to severe chronic kidney dise

  1. THE SYMPATHETIC NERVOUS SYSTEM ALTERATIONS IN HUMAN HYPERTENSION

    Science.gov (United States)

    Grassi, Guido; Mark, Allyn; Esler, Murray

    2015-01-01

    A number of articles have dealt with the importance and mechanisms of the sympathetic nervous system alterations in experimental animal models of hypertension. This review addresses the role of the sympathetic nervous system in the pathophysiology and therapy of human hypertension. We first discuss the strengths and limitations of various techniques for assessing the sympathetic nervous system in humans, with a focus on heart rate, plasma norepinephrine, microneurographic recording of sympathetic nerve traffic, and measurements of radiolabeled norepinephrine spillover. We then examine the evidence supporting the importance of neuroadrenergic factors as “promoters” and “amplifiers” of human hypertension. We expand on the role of the sympathetic nervous system in two increasingly common forms of secondary hypertension, namely hypertension associated with obesity and with renal disease. With this background, we examine interventions of sympathetic deactivation as a mode of antihypertensive treatment. Particular emphasis is given to the background and results of recent therapeutic approaches based on carotid baroreceptor stimulation and radiofrequency ablation of the renal nerves. PMID:25767284

  2. Potential lifetime cost-effectiveness of catheter-based renal sympathetic denervation in patients with resistant hypertension.

    Science.gov (United States)

    Dorenkamp, Marc; Bonaventura, Klaus; Leber, Alexander W; Boldt, Julia; Sohns, Christian; Boldt, Leif-Hendrik; Haverkamp, Wilhelm; Frei, Ulrich; Roser, Mattias

    2013-02-01

    Recent studies have demonstrated the safety and efficacy of catheter-based renal sympathetic denervation (RDN) for the treatment of resistant hypertension. We aimed to determine the cost-effectiveness of this approach separately for men and women of different ages. A Markov state-transition model accounting for costs, life-years, quality-adjusted life-years (QALYs), and incremental cost-effectiveness was developed to compare RDN with best medical therapy (BMT) in patients with resistant hypertension. The model ran from age 30 to 100 years or death, with a cycle length of 1 year. The efficacy of RDN was modelled as a reduction in the risk of hypertension-related disease events and death. Analyses were conducted from a payer's perspective. Costs and QALYs were discounted at 3% annually. Both deterministic and probabilistic sensitivity analyses were performed. When compared with BMT, RDN gained 0.98 QALYs in men and 0.88 QALYs in women 60 years of age at an additional cost of €2589 and €2044, respectively. As the incremental cost-effectiveness ratios increased with patient age, RDN consistently yielded more QALYs at lower costs in lower age groups. Considering a willingness-to-pay threshold of €35 000/QALY, there was a 95% probability that RDN would remain cost-effective up to an age of 78 and 76 years in men and women, respectively. Cost-effectiveness was influenced mostly by the magnitude of effect of RDN on systolic blood pressure, the rate of RDN non-responders, and the procedure costs of RDN. Renal sympathetic denervation is a cost-effective intervention for patients with resistant hypertension. Earlier treatment produces better cost-effectiveness ratios.

  3. Pulmonary vein isolation alone and combined with renal sympathetic denervation in chronic kidney disease patients with refractory atrial fibrillation.

    Science.gov (United States)

    Kiuchi, Márcio G; Chen, Shaojie; E Silva, Gustavo R; Paz, Luis M R; Kiuchi, Tetsuaki; de Paula Filho, Ary G; Souto, Gladyston L L

    2016-12-01

    Atrial fibrillation (AF) commonly occurs in association with chronic kidney disease (CKD), resulting in adverse outcomes. Combining pulmonary vein isolation (PVI) and renal sympathetic denervation (RSD) may reduce the recurrence of AF in patients with CKD and hypertension. We considered that RSD could reduce the recurrence of AF in patients with CKD by modulating sympathetic hyperactivity. Our goal was to compare the impact of PVI + RSD with that of PVI alone in patients with concurrent AF and CKD. This was a single-center, prospective, longitudinal, randomized, double-blind study. Forty-five patients with controlled hypertension, symptomatic paroxysmal AF and/or persistent AF, stage 2 or 3 CKD, and a dual-chamber pacemaker were enrolled from January 2014 to January 2015. We assessed the 30-second recurrence of AF recorded by the pacemaker, 24-hour ambulatory blood pressure measurements, estimated glomerular filtration rate, albuminuria, echocardiographic parameters, and safety of RSD. No patient developed procedural or other complications. The ambulatory blood pressure measurements did not differ within the PVI + RSD group or between the PVI + RSD and PVI groups throughout the study. Significantly more patients in the PVI + RSD group than in the PVI group were free of AF at the 12-month follow-up evaluation. The PVI group had an unacceptable response to ablation with respect to changes in echocardiographic parameters, whereas these parameters improved in the PVI + RSD group. PVI + RSD were associated with a lower AF recurrence rate than PVI alone; it also improved renal function and some echocardiographic parameters. These encouraging data will serve as baseline information for further long-term studies on larger patient populations.

  4. Enhanced adipose afferent reflex contributes to sympathetic activation in diet-induced obesity hypertension.

    Science.gov (United States)

    Xiong, Xiao-Qing; Chen, Wei-Wei; Han, Ying; Zhou, Ye-Bo; Zhang, Feng; Gao, Xing-Ya; Zhu, Guo-Qing

    2012-11-01

    We recently found that adipose afferent reflex (AAR) induced by chemical stimulation of white adipose tissue (WAT) increased sympathetic outflow and blood pressure in normal rats. The study was designed to test the hypothesis that AAR contributes to sympathetic activation in obesity hypertension. Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Stimulation of WAT with capsaicin increased renal sympathetic nerve activity and mean arterial pressure. Both AAR and WAT afferent activity were enhanced in obesity hypertension (OH) compared with obesity nonhypertension (ON) and in ON compared with obesity-resistant or control diet rats. WAT sensory denervation induced by resiniferatoxin caused greater decreases in renal sympathetic nerve activity and mean arterial pressure in OH than ON and in ON than obesity-resistant or control. The depressor effect of resiniferatoxin lasted ≥ 3 weeks in OH. Leptin antagonist in WAT reduced renal sympathetic nerve activity and mean arterial pressure in OH. WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats. Inhibiting paraventricular nucleus neurons with lidocaine attenuated renal sympathetic nerve activity in OH and ON, decreased mean arterial pressure in OH, and abolished the capsaicin-induced AAR in all groups. The results indicate that enhanced AAR contributes to sympathetic activation in OH, and paraventricular nucleus plays an important role in the enhanced AAR and sympathetic activation in OH.

  5. Sympathetic nervous activity and renal and systemic hemodynamics in cirrhosis: plasma norepinephrine concentration, hepatic extraction, and renal release

    DEFF Research Database (Denmark)

    Ring-Larsen, H; Hesse, B; Henriksen, Jens Henrik Sahl

    1982-01-01

    Systemic and renal neurovascular reactivity was investigated in eight patients with cirrhosis and in eight control subjects with fatty liver during postural changes. In the supine position, mean renal blood flow averaged 1.51 and 2.97 ml per gm per min in patients and controls, respectively (p less...... 60 degrees head-up tilt, the increase in NE was similar in both groups. In another 10 patients with cirrhosis in recumbency, the splanchnic arterial-hepatic venous extraction of NE averaged 0.43 (p less than 0.01), and the hepatic clearance of NE averaged 315 ml per min which is of the same order...... be responsible for renal vasoconstriction in these patients. However, systemic and renal neurovascular reactivity seems to be maintained even at an advanced stage of the disease....

  6. A microcontroller-based telemetry system for sympathetic nerve activity and ECG measurement.

    Science.gov (United States)

    Harada, E; Yonezawa, Y; Caldwell, W M; Hahn, A W

    1999-01-01

    A telemetry system employing a low power 8-bit microcontroller has been developed for chronic unanesthetized small animal studies. The two-channel system is designed for use with animals in shielded cages. Analog signals from implantable ECG and nerve electrodes are converted to an 8-bit serial digital format. This is accomplished by individual 8 bit A/D converters included in the microcontroller, which also has serial I/O port. The converted serial binary code is applied directly to an antenna wire. Therefore, the system does not need to employ a separate transmitter, such as in FM or infrared optical telemeters. The system is used in a shielded animal cage to reduce interference from external radio signals and 60 Hz power line fields. The code is received by a high input impedance amplifier in the cage and is then demodulated. The telemeter is powered by a small 3 V lithium battery, which provides 100 hours of continuous operation. The circuit is constructed on two 25 x 25 mm. printed circuit boards and encapsulated in epoxy, yielding a total volume of 6.25 cc. The weight is 15 g.

  7. Assessment of cardiac sympathetic nerve activity in children with chronic heart failure using quantitative iodine-123 metaiodobenzylguanidine imaging

    Energy Technology Data Exchange (ETDEWEB)

    Karasawa, Kensuke; Ayusawa, Mamoru; Noto, Nobutaka; Sumitomo, Naokata; Okada, Tomoo; Harada, Kensuke [Nihon Univ., Tokyo (Japan). School of Medicine

    2000-12-01

    Cardiac sympathetic nerve activity in children with chronic heart failure was examined by quantitative iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging in 33 patients aged 7.5{+-}6.1 years (range 0-18 years), including 8 with cardiomyopathy, 15 with congenital heart disease, 3 with anthracycrine cardiotoxicity, 3 with myocarditis, 3 with primary pulmonary hypertension and 1 with Pompe's disease. Anterior planar images were obtained 15 min and 3 hr after the injection of iodine-123 MIBG. The cardiac iodine-123 MIBG uptake was assessed as the heart to upper mediastinum uptake activity ratio of the delayed image (H/M) and the cardiac percentage washout rate (%WR). The severity of chronic heart failure was class I (no medication) in 8 patients, class II (no symptom with medication) in 9, class III (symptom even with medication) in 10 and class IV (late cardiac death) in 6. H/M was 2.33{+-}0.22 in chronic heart failure class I, 2.50{+-}0.34 in class II, 1.95{+-}0.61 in class III, and 1.39{+-}0.29 in class IV (p<0.05). %WR was 24.8{+-}12.8% in chronic heart failure class I, 23.3{+-}10.2% in class II, 49.2{+-}24.5% in class III, and 66.3{+-}26.5% in class IV (p<0.05). The low H/M and high %WR were proportionate to the severity of chronic heart failure. Cardiac iodine-123 MIBG showed cardiac adrenergic neuronal dysfunction in children with severe chronic heart failure. Quantitative iodine-123 MIBG myocardial imaging is clinically useful as a predictor of therapeutic outcome and mortality in children with chronic heart failure. (author)

  8. Sympathetic fibre sprouting in the skin contributes to pain-related behaviour in spared nerve injury and cuff models of neuropathic pain.

    Science.gov (United States)

    Nascimento, Francisney P; Magnussen, Claire; Yousefpour, Noosha; Ribeiro-da-Silva, Alfredo

    2015-09-17

    Cuff and spared nerve injury (SNI) in the sciatic territory are widely used to model neuropathic pain. Because nociceptive information is first detected in skin, it is important to understand how alterations in peripheral innervation contribute to pain in each model. Over 16 weeks in male rats, changes in sensory and autonomic innervation of the skin were described after cuff and SNI using immunohistochemistry to label myelinated (neurofilament 200 positive-NF200+) and peptidergic (calcitonin gene-related peptide positive-CGRP+) primary afferents and sympathetic fibres (dopamine β-hydroxylase positive-DBH+) Cuff and SNI caused an early loss and later reinnervation of NF200 and CGRP fibres in the plantar hind paw skin. In both models, DBH+ fibres sprouted into the upper dermis of the plantar skin 4 and 6 weeks after injury. Despite these similarities, behavioural pain measures were significantly different in each model. Sympathectomy using guanethidine significantly alleviated mechanical allodynia 6 weeks after cuff, when peak sympathetic sprouting was observed, having no effect at 2 weeks, when fibres were absent. In SNI animals, mechanical allodynia in the lateral paw was significantly improved by guanethidine at 2 and 6 weeks, and the development of cold hyperalgesia, which roughly paralleled the appearance of ectopic sympathetic fibres, was alleviated by guanethidine at 6 weeks. Sympathetic fibres did not sprout into the dorsal root ganglia at 2 or 6 weeks, indicating their unimportance to pain behaviour in these two models. Alterations in sympathetic innervation in the skin represents an important mechanism that contributes to pain in cuff and SNI models of neuropathic pain.

  9. Involvement of presynaptic voltage-dependent Kv3 channel in endothelin-1-induced inhibition of noradrenaline release from rat gastric sympathetic nerves.

    Science.gov (United States)

    Nakamura, Kumiko; Shimizu, Takahiro; Tanaka, Kenjiro; Taniuchi, Keisuke; Yokotani, Kunihiko

    2012-11-05

    We previously reported that two types of K(+) channels, the BK type Ca(2+)-activated K(+) channel coupled with phospholipase C (PLC) and the voltage-dependent K(+) channel (Kv channel), are, respectively, involved in the prostanoid TP receptor- and muscarinic M(2) receptor-mediated inhibition of noradrenaline (NA) release from rat gastric sympathetic nerves. In the present study, therefore, we examined whether these K(+) channels are involved in endothelin-1-induced inhibition of NA release, using an isolated, vascularly perfused rat stomach. The gastric sympathetic postganglionic nerves around the left gastric artery were electrically stimulated twice at 2.5 Hz for 1 min, and endothelin-1 was added during the second stimulation. Endothelin-1 (1, 2 and 10 nM) dose-dependently inhibited gastric NA release. Endothelin-1 (2 nM)-induced inhibition of NA release was neither attenuated by PLC inhibitors [U-73122 (3 μM) and ET-18-OCH(3) (3 μM)] nor by Ca(2+)-activated K(+) channel blockers [charybdotoxin (0.1 μM) (a blocker of BK type K(+) channel) and apamin (0.3 μM) (a blocker of SK type K(+) channel)]. The endothelin-1-induced inhibitory response was also not attenuated by α-dendrotoxin (0.1 μM) (a selective inhibitor of Kv1 channel), but abolished by 4-aminopyridine (20 μM) (a selectively inhibitory dose for Kv3 channel). These results suggest the involvement of a voltage-dependent Kv3 channel in the endothelin-1-induced inhibition of NA release from the gastric sympathetic nerves in rats.

  10. Exuberant sprouting of sensory and sympathetic nerve fibers in nonhealed bone fractures and the generation and maintenance of chronic skeletal pain.

    Science.gov (United States)

    Chartier, Stephane R; Thompson, Michelle L; Longo, Geraldine; Fealk, Michelle N; Majuta, Lisa A; Mantyh, Patrick W

    2014-11-01

    Skeletal injury is a leading cause of chronic pain and long-term disability worldwide. While most acute skeletal pain can be effectively managed with nonsteroidal anti-inflammatory drugs and opiates, chronic skeletal pain is more difficult to control using these same therapy regimens. One possibility as to why chronic skeletal pain is more difficult to manage over time is that there may be nerve sprouting in nonhealed areas of the skeleton that normally receive little (mineralized bone) to no (articular cartilage) innervation. If such ectopic sprouting did occur, it could result in normally nonnoxious loading of the skeleton being perceived as noxious and/or the generation of a neuropathic pain state. To explore this possibility, a mouse model of skeletal pain was generated by inducing a closed fracture of the femur. Examined animals had comminuted fractures and did not fully heal even at 90+days post fracture. In all mice with nonhealed fractures, exuberant sensory and sympathetic nerve sprouting, an increase in the density of nerve fibers, and the formation of neuroma-like structures near the fracture site were observed. Additionally, all of these animals exhibited significant pain behaviors upon palpation of the nonhealed fracture site. In contrast, sprouting of sensory and sympathetic nerve fibers or significant palpation-induced pain behaviors was never observed in naïve animals. Understanding what drives this ectopic nerve sprouting and the role it plays in skeletal pain may allow a better understanding and treatment of this currently difficult-to-control pain state. Copyright © 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

  11. Acute beetroot juice supplementation on sympathetic nerve activity: a randomized, double-blind, placebo-controlled proof-of-concept study.

    Science.gov (United States)

    Notay, Karambir; Incognito, Anthony V; Millar, Philip J

    2017-07-01

    Acute dietary nitrate ([Formula: see text]) supplementation reduces resting blood pressure in healthy normotensives. This response has been attributed to increased nitric oxide bioavailability and peripheral vasodilation, although nitric oxide also tonically inhibits central sympathetic outflow. We hypothesized that acute dietary [Formula: see text] supplementation using beetroot (BR) juice would reduce blood pressure and muscle sympathetic nerve activity (MSNA) at rest and during exercise. Fourteen participants (7 men and 7 women, age: 25 ± 10 yr) underwent blood pressure and MSNA measurements before and after (165-180 min) ingestion of 70ml high-[Formula: see text] (~6.4 mmol [Formula: see text]) BR or [Formula: see text]-depleted BR placebo (PL; ~0.0055 mmol [Formula: see text]) in a double-blind, randomized, crossover design. Blood pressure and MSNA were also collected during 2 min of static handgrip (30% maximal voluntary contraction). The changes in resting MSNA burst frequency (-3 ± 5 vs. 3 ± 4 bursts/min, P = 0.001) and burst incidence (-4 ± 7 vs. 4 ± 5 bursts/100 heart beats, P = 0.002) were lower after BR versus PL, whereas systolic blood pressure (-1 ± 5 vs. 2 ± 5 mmHg, P = 0.30) and diastolic blood pressure (4 ± 5 vs. 5 ± 7 mmHg, P = 0.68) as well as spontaneous arterial sympathetic baroreflex sensitivity (P = 0.95) were not different. During static handgrip, the change in MSNA burst incidence (1 ± 8 vs. 8 ± 9 bursts/100 heart beats, P = 0.04) was lower after BR versus PL, whereas MSNA burst frequency (6 ± 6 vs. 11 ± 10 bursts/min, P = 0.11) as well as systolic blood pressure (11 ± 7 vs. 12 ± 8 mmHg, P = 0.94) and diastolic blood pressure (11 ± 4 vs. 11 ± 4 mmHg, P = 0.60) were not different. Collectively, these data provide proof of principle that acute BR supplementation can decrease central sympathetic outflow at rest and during exercise. Dietary [Formula: see text] supplementation may represent a novel intervention to target

  12. 去肾交感神经支配术与高血压%Renal sympathetic denervation for the treatment of hypertension

    Institute of Scientific and Technical Information of China (English)

    杨宁; 程康安; 李拥军

    2012-01-01

    Although effective antihypertensive drug together with lifestyle intervention has been widely employed in the medical field, essential hypertension remains one of the main diseases affecting human being's health. Because of some reasons such as lower rate of patients' awareness of hypertension, lower rate of receiving treatment, poor tolerance to the antihypertensive drugs, patient'g poor biddable willing, unreasonable medication, etc. about one third of the patients having essential hypertension are not be able to effectively control their blood pressure level and they have been in a high risk status to cardio - cerebral vascular diseases all along. Therefore, it is very urgent to find out a safer and more effective therapy for essential hypertension. Renal sympathetic denervation (RSD) has been recently employed in clinical practice for hypertension. This, therapy is based on the catheterization technique combined with the radiofrequency ablation to selectively destroy the targeted renal nerves in order to treat the intractable essential hypertension. Two clinical trials, Symplicity HTN -1 and HTN -2, have been conducted to evaluate the feasibility and effectiveness of RSD, and the results provide reliable evidence, which indicates that RSD is safe and effective in clinical use. This paper aims to make a brief introduction of the recent research progress concerning the safety and efficacy of RSD technique.(J Intervent Radiol, 2012, 21: 441-446)%目前,原发性高血压及其并发症仍是影响人类健康的主要疾病之一.原发性高血压因其知晓率低和治疗率低、药物不耐受、患者依从性差以及不合理用药等原因,有近1/3患者不能有效控制血压,处在心脑血管疾病高危状态.为此,寻求更为安全和有效的治疗高血压的方法十分迫切.去肾交感神经支配术基于导管方法应用射频消融选择性靶向损毁肾交感神经,以达到治疗顽固性高血压的目的.

  13. Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin-angiotensin system.

    Science.gov (United States)

    Maranon, Rodrigo O; Reckelhoff, Jane F

    2016-02-01

    Hypertension in postmenopausal women is less well controlled than in age-matched men. The aging female SHR is a model of postmenopausal hypertension that is mediated in part by activation of the renin-angiotensin system (RAS) and by the renal sympathetic nervous system. In this study, the hypothesis was tested that renal denervation would lower the blood pressure in old female SHR and would attenuate the antihypertensive effects of AT1 receptor antagonism. Retired breeder female SHR were subjected to right uninephrectomy (UNX) and left renal denervation (RD) or UNX and sham, and 2 weeks later, baseline mean arterial pressure (MAP; radiotelemetry) was measured for 4 days, and then rats were treated with angiotensin (AT1) receptor antagonist, losartan (40 mg/kg/day po) for 6 days. Renal denervation reduced MAP in old females compared to sham (172 ± 6 vs. 193 ± 6 mm Hg; P system and the RAS have independent effects to control the blood pressure in old female SHR. Since the denervated rats treated with losartan remained hypertensive, the data also suggest that other mechanisms than the RAS and renal sympathetic nervous system contribute to the hypertension in old female SHR. The data also suggest that multiple mechanisms may mediate the elevated blood pressure in postmenopausal women.

  14. Effects of perindopril on cardiac sympathetic nerve activity in patients with congestive heart failure: comparison with enalapril

    Energy Technology Data Exchange (ETDEWEB)

    Kasama, Shu; Toyama, Takuji; Suzuki, Tadashi; Kurabayashi, Masahiko [Gunma University School of Medicine, Department of Cardiovascular Medicine, Maebashi, Gunma (Japan); Kumakura, Hisao; Takayama, Yoshiaki; Ichikawa, Shuichi [Cardiovascular Hospital of Central Japan, Department of Internal Medicine, Gunma (Japan)

    2005-08-01

    The production of aldosterone in the heart is suppressed by the angiotensin-converting enzyme (ACE) inhibitor perindopril in patients with congestive heart failure (CHF). Moreover, perindopril has been reported to have more cardioprotective effects than enalapril. Forty patients with CHF [left ventricular ejection fraction (LVEF) <45%; mean 33{+-}7%] were randomly assigned to perindopril (2 mg/day; n=20) or enalapril (5 mg/day; n=20). All patients were also treated with diuretics. The delayed heart/mediastinum count (H/M) ratio, delayed total defect score (TDS) and washout rate (WR) were determined from {sup 123}I-meta-iodobenzylguanidine (MIBG) images, and plasma brain natriuretic peptide (BNP) concentrations were measured before and 6 months after treatment. The left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and LVEF were also determined by echocardiography. After treatment, in patients receiving perindopril, TDS decreased from 39{+-}10 to 34{+-}9 (P<0.01), H/M ratios increased from 1.62{+-}0.27 to 1.76{+-}0.29 (P<0.01), WR decreased from 50{+-}14% to 42{+-}14% (P<0.05) and plasma BNP concentrations decreased from 226{+-}155 to 141{+-}90 pg/ml (P<0.0005). In addition, the LVEDV decreased from 180{+-}30 to 161{+-}30 ml (P<0.05) and the LVESV decreased from 122{+-}35 to 105{+-}36 ml (P<0.05). Although the LVEF tended to increase, the change was not statistically significant (from 33{+-}8% to 36{+-}12%; P=NS). On the other hand, there were no significant changes in these parameters in patients receiving enalapril. Plasma BNP concentrations, {sup 123}I-MIBG scintigraphic and echocardiographic parameters improved after 6 months of perindopril treatment. These findings indicate that perindopril treatment can ameliorate the cardiac sympathetic nerve activity and the left ventricular performance in patients with CHF. (orig.)

  15. Roles of estrogen and progesterone in modulating renal nerve function in the rat kidney

    Energy Technology Data Exchange (ETDEWEB)

    Graceli, J.B. [Departamento de Morfologia, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES (Brazil); Cicilini, M.A.; Bissoli, N.S.; Abreu, G.R.; Moysés, M.R. [Departamento de Ciências Fisiológicas, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES (Brazil)

    2013-07-02

    The maintenance of extracellular Na{sup +} and Cl{sup -} concentrations in mammals depends, at least in part, on renal function. It has been shown that neural and endocrine mechanisms regulate extracellular fluid volume and transport of electrolytes along nephrons. Studies of sex hormones and renal nerves suggested that sex hormones modulate renal function, although this relationship is not well understood in the kidney. To better understand the role of these hormones on the effects that renal nerves have on Na{sup +} and Cl{sup -} reabsorption, we studied the effects of renal denervation and oophorectomy in female rats. Oophorectomized (OVX) rats received 17β-estradiol benzoate (OVE, 2.0 mg·kg{sup -1}·day{sup -1}, sc) and progesterone (OVP, 1.7 mg·kg{sup -1}·day{sup -1}, sc). We assessed Na{sup +} and Cl{sup -} fractional excretion (FE{sub Na{sup {sub +}}} and FE{sub Cl{sup {sub -}}}, respectively) and renal and plasma catecholamine release concentrations. FE{sub Na{sup {sub +}}}, FE{sub Cl{sup {sub -}}}, water intake, urinary flow, and renal and plasma catecholamine release levels increased in OVX vs control rats. These effects were reversed by 17β-estradiol benzoate but not by progesterone. Renal denervation did not alter FE{sub Na{sup {sub +}}}, FE{sub Cl{sup {sub -}}}, water intake, or urinary flow values vs controls. However, the renal catecholamine release level was decreased in the OVP (236.6±36.1 ng/g) and denervated rat groups (D: 102.1±15.7; ODE: 108.7±23.2; ODP: 101.1±22.1 ng/g). Furthermore, combining OVX + D (OD: 111.9±25.4) decreased renal catecholamine release levels compared to either treatment alone. OVE normalized and OVP reduced renal catecholamine release levels, and the effects on plasma catecholamine release levels were reversed by ODE and ODP replacement in OD. These data suggest that progesterone may influence catecholamine release levels by renal innervation and that there are complex interactions among renal nerves, estrogen

  16. Ang II enhances noradrenaline release from sympathetic nerve endings thus contributing to the up-regulation of metalloprotease-2 in aortic dissection patients' aorta wall.

    Directory of Open Access Journals (Sweden)

    Zhipeng Hu

    Full Text Available OBJECT: To test the hypothesis that angiotensin II (Ang II could enhance noradrenaline (NA release from sympathetic nerve endings of the aorta thus contributing to the up-regulation of matrix metalloproteinase 2 (MMP-2 during the formation of aortic dissection (AD. METHODS: Ang II, NA, MMP-2, MMP-9 of the aorta sample obtained during operation from aortic dissection patients were detected by High Performance Liquid Chromatography and ELISA and compared with controls. Isotope labelling method was used to test the impact of exogenous Ang II and noradrenaline on the NA release and MMP-2, MMP-9 expression on Sprague Dawley (SD rat aorta rings in vitro. Two kidneys, one clip, models were replicated for further check of that impact in SD rats in vivo. RESULTS: The concentration of Ang II, MMP-2, 9 was increased and NA concentration was decreased in aorta samples from AD patients. Exogenous Ang II enhanced while exogenous NA restrained NA release from aortic sympathetic endings. The Ang II stimulated NA release and the following MMP-2 up-regulation could be weakened by Losartan and chemical sympathectomy. Beta blocker did not influence NA release but down-regulated MMP-2. Long term in vivo experiments confirmed that Ang II could enhance NA release and up-regulate MMP-2. CONCLUSIONS: AD is initiated by MMP-2 overexpression as a result of increased NA release from sympathetic nervous endings in response to Ang II. This indicates an interaction of RAS and SAS during the formation of AD.

  17. Heterogeneous blood flow distribution within single skeletal muscles in the rabbit: role of vasomotion, sympathetic nerve activity and effect of vasodilation.

    Science.gov (United States)

    Iversen, P O; Nicolaysen, G

    1989-09-01

    A major heterogeneous distribution of blood flow has been described on a non-microvascular level within single skeletal muscles at rest and during exercise hyperaemia both in the dog and in the rabbit. The heterogeneity in blood flow distribution could be composed of both a steady-state region-to-region variability (spatial) and a time-dependent variability (temporal) in blood flow to each region. In the present study we estimated their relative contributions to the variations in blood flow within the muscles. Furthermore, we determined whether sympathetic nerve activity contributed to and whether pharmacologically induced vasodilation affected the heterogeneous blood flow pattern. Regional blood flow measurements were based on microsphere infusions into anaesthetized rabbits. Blood flow was determined under both resting conditions and during exercise hyperaemia in regions weighing 0.25 g each within hind leg muscles. The coefficient of variation for the spatial variability was twice that of the temporal one: 0.32 and 0.16 (mean) respectively. Neither stimulation of the sympathetic nerves, sympathectomy nor vasodilation affected the heterogeneity in blood flow. When exercise hyperaemia was induced, blood flow increased in all regions so that a positive (P less than 0.05) correlation was present between resting and exercising blood flow values in the individual regions. Although regional variation in vascularization could explain the observations during exercise hyperaemia, we have at present no fully satisfying explanation for the observed regional heterogeneity in blood flow.

  18. Targeted P2X7 R shRNA delivery attenuates sympathetic nerve sprouting and ameliorates cardiac dysfunction in rats with myocardial infarction.

    Science.gov (United States)

    Gao, Hongmei; Yin, Jie; Shi, Yugen; Hu, Hesheng; Li, Xiaolu; Xue, Mei; Cheng, Wenjuan; Wang, Ye; Li, Xinran; Li, Yongkang; Wang, Yu; Yan, Suhua

    2017-04-01

    Inflammation-dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in the etiology of arrhythmias resulting in sudden cardiac death; however, the mechanisms responsible remain to be elucidated. Although P2X7 R is a key immune mediator, its role has yet to be explored. We investigated whether P2X7 R regulates NF-κB and affects cardiac sympathetic reinnervation in rats undergoing MI. An adenoviral vector with a short hairpin RNA (shRNA) sequence inserted was adopted for the inhibition of P2X7 R in vivo. Myocardial infarction was induced by left coronary artery ligation, and immediately after that, recombinant P2X7 R-shRNA adenovirus, negative adenovirus (control), or normal saline solution (vehicle) was injected intramyocardially around the MI region and border areas. A high level of P2X7 R was activated in the infarcted tissue at an early stage. The administration of P2X7 R RNAi resulted in the inhibition of Akt and Erk1/2 phosphorylation and decreased the activation of NF-κB and macrophage infiltration, as well as attenuated the expression of nerve growth factor (NGF). Eventually, the NGF-induced sympathetic hyperinnervation was blunted, as assessed by the immunofluorescence of tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP 43). At 7 days post-MI, the arrhythmia score of programmed electrical stimulation in the vehicle-treated infarcted rats was higher than the MI-shRNA group. Further amelioration of cardiac dysfunction was also detected. The administration of P2X7 R RNAi during the acute inflammatory response phase prevented the process of sympathetic hyperinnervation after MI, which was associated in part with inhibiting the Akt and ERK1/2 pathways and NF-κB activation. © 2016 John Wiley & Sons Ltd.

  19. The role of plasma volume, plasma renin and the sympathetic nervous system in the posture-induced decline in renal lithium clearance in man.

    Science.gov (United States)

    Smith, D F; Shimizu, M

    1978-01-01

    Excretion of lithium in urine was studied in 2 healthy males while recumbent and while upright, either walking or standing quietly. An oral dose of 24.3 mmol of Lit was taken as three lithium carbonate tablets 13 h before clearance tests. Renal lithium clearance decreased and lithium fractional reabsorption increased while upright. Standing immersed to the neck in water, which prevents the fall in plasma volume upon changing posture from recumbent to upright, prevented the fall in renal lithium clearance as well as the rise in lithium fractional reabsorption while upright. Oral doses of guanethidine (total dose of 200 mg) or oxprenolol (total dose of 140 mg) taken to prevent high levels of sympathetic nervous system activity and plasma renin, respectively, failed to prevent the fall in renal lithium clearance or the rise in lithium fractional reabsorption upon changing posture from recumbent to upright. The findings indicate that the fall in renal lithium clearance and the rise in lithium fractional reabsorption upon changing posture from recumbent to upright is related to the fall in plasma volume but not to high levels of sympathetic nervous system activity or plasma renin activity.

  20. Moxonidine prevents ischemia/reperfusion-induced renal injury in rats.

    Science.gov (United States)

    Tsutsui, Hidenobu; Sugiura, Takahiro; Hayashi, Kentaro; Ohkita, Mamoru; Takaoka, Masanori; Yukimura, Tokihito; Matsumura, Yasuo

    2009-01-28

    Enhancement of renal sympathetic nerve activity during renal ischemia and its consequent effect on norepinephrine overflow from nerve endings after reperfusion play important roles in the development of ischemic acute kidney injury. In the present study, we evaluated whether moxonidine, an alpha(2)-adrenaline/I(1)-imidazoline receptor agonist which is known to elicit sympathoinhibitory action, would prevent the post-ischemic renal injury. Ischemic acute kidney injury was induced by clamping the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after contralateral nephrectomy. Intravenous (i.v.) injection of moxonidine at a dose of 360 nmol/kg to ischemic acute kidney injury rats suppressed the enhanced renal sympathetic nerve activity during the ischemic period, to a degree similar to findings with intracerebroventricular (i.c.v.) injection of moxonidine at a dose of 36 nmol/kg. On the other hand, suppressive effects of the i.v. treatment on renal venous norepinephrine overflow, renal dysfunction and tissue injury in the post-ischemic kidney were significantly greater than those elicited by the i.c.v. treatment. These results suggest that renoprotective effects of moxonidine on ischemic acute kidney injury probably result from its suppressive action on the ischemia-enhanced renal sympathetic nerve activity followed by norepinephrine spillover from the nerve endings of the post-ischemic kidney.

  1. β3 adrenergic receptor in the kidney may be a new player in sympathetic regulation of renal function.

    Science.gov (United States)

    Procino, Giuseppe; Carmosino, Monica; Milano, Serena; Dal Monte, Massimo; Schena, Giorgia; Mastrodonato, Maria; Gerbino, Andrea; Bagnoli, Paola; Svelto, Maria

    2016-09-01

    To date, the study of the sympathetic regulation of renal function has been restricted to the important contribution of β1- and β2-adrenergic receptors (ARs). Here we investigate the expression and the possible physiologic role of β3-adrenergic receptor (β3-AR) in mouse kidney. The β3-AR is expressed in most of the nephron segments that also express the type 2 vasopressin receptor (AVPR2), including the thick ascending limb and the cortical and outer medullary collecting duct. Ex vivo experiments in mouse kidney tubules showed that β3-AR stimulation with the selective agonist BRL37344 increased intracellular cAMP levels and promoted 2 key processes in the urine concentrating mechanism. These are accumulation of the water channel aquaporin 2 at the apical plasma membrane in the collecting duct and activation of the Na-K-2Cl symporter in the thick ascending limb. Both effects were prevented by the β3-AR antagonist L748,337 or by the protein kinase A inhibitor H89. Interestingly, genetic inactivation of β3-AR in mice was associated with significantly increased urine excretion of water, sodium, potassium, and chloride. Stimulation of β3-AR significantly reduced urine excretion of water and the same electrolytes. Moreover, BRL37344 promoted a potent antidiuretic effect in AVPR2-null mice. Thus, our findings are of potential physiologic importance as they uncover the antidiuretic effect of β3-AR stimulation in the kidney. Hence, β3-AR agonism might be useful to bypass AVPR2-inactivating mutations. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

  2. Adjusted drug treatment is superior to renal sympathetic denervation in patients with true treatment-resistant hypertension.

    Science.gov (United States)

    Fadl Elmula, Fadl Elmula M; Hoffmann, Pavel; Larstorp, Anne C; Fossum, Eigil; Brekke, Magne; Kjeldsen, Sverre E; Gjønnæss, Eyvind; Hjørnholm, Ulla; Kjaer, Vibeke N; Rostrup, Morten; Os, Ingrid; Stenehjem, Aud; Høieggen, Aud

    2014-05-01

    We aimed to investigate for the first time the blood pressure (BP)-lowering effect of renal sympathetic denervation (RDN) versus clinically adjusted drug treatment in true treatment-resistant hypertension (TRH) after excluding patients with confounding poor drug adherence. Patients with apparent TRH (n=65) were referred for RDN, and those with secondary and spurious hypertension (n=26) were excluded. TRH was defined as office systolic BP (SBP) >140 mm Hg, despite maximally tolerated doses of ≥3 antihypertensive drugs including a diuretic. In addition, ambulatory daytime SBP >135 mm Hg after witnessed intake of antihypertensive drugs was required, after which 20 patients had normalized BP and were excluded. Patients with true TRH were randomized and underwent RDN (n=9) performed with Symplicity Catheter System versus clinically adjusted drug treatment (n=10). The study was stopped early for ethical reasons because RDN had uncertain BP-lowering effect. Office SBP and diastolic BP in the drug-adjusted group changed from 160±14/88±13 mm Hg (±SD) at baseline to 132±10/77±8 mm Hg at 6 months (Pdrug-adjusted group at 6 months (P=0.002 and P=0.004, respectively), and absolute changes in SBP were larger in the drug-adjusted group (P=0.008). Ambulatory BPs changed in parallel to office BPs. Our data suggest that adjusted drug treatment has superior BP lowering effects compared with RDN in patients with true TRH. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT01673516.

  3. Central PACAP mediates the sympathetic effects of leptin in a tissue-specific manner.

    Science.gov (United States)

    Tanida, M; Hayata, A; Shintani, N; Yamamoto, N; Kurata, Y; Shibamoto, T; Morgan, D A; Rahmouni, K; Hashimoto, H

    2013-05-15

    We previously demonstrated that the peptidergic neurotransmitter pituitary adenylate cyclase-activating polypeptide (PACAP) affects the autonomic system and contributes to the control of metabolic and cardiovascular functions. Previous studies have demonstrated the importance of centrally-mediated sympathetic effects of leptin for obesity-related hypertension. Here we tested whether PACAP signaling in the brain is implicated in leptin-induced sympathetic excitation and appetite suppression. In anesthetized mice, intracerebroventricular (ICV) pre-treatment with PACAP6-38, an antagonist of the PACAP receptors (PAC1-R and VPAC2), inhibited the increase in white adipose tissue sympathetic nerve activity (WAT-SNA) produced by ICV leptin (2μg). In contrast, leptin-induced stimulation of renal sympathetic nerve activity (RSNA) was not affected by ICV pre-treatment with PACAP6-38. Moreover, in PACAP-deficient (Adcyap1-/-) mice, ICV leptin-induced WAT-SNA increase was impaired, whereas RSNA response was preserved. The reductions in food intake and body weight evoked by ICV leptin were attenuated in Adcyap1-/- mice. Our data suggest that hypothalamic PACAP signaling plays a key role in the control by leptin of feeding behavior and lipocatabolic sympathetic outflow, but spares the renal sympathetic traffic. Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

  4. Effects of cilnidipine on sympathetic nerve activity and cardiorenal function in hypertensive patients with type 2 diabetes mellitus: association with BNP and aldosterone levels.

    Science.gov (United States)

    Tanaka, Masami; Sekioka, Risa; Nishimura, Takeshi; Ichihara, Atsuhiro; Itoh, Hiroshi

    2014-12-01

    Hypertension stimulates the sympathetic nervous system and this phenomenon is exacerbated by diabetes mellitus. We investigated the effects of cilnidipine, an N/L-type calcium channel blocker, on aspects of this system in patients with type 2 diabetes mellitus. In 33 hypertensive patients with type 2 diabetes mellitus treated with a calcium channel blocker other than cilnidipine, we evaluated the influence of switching to cilnidipine on blood pressure, heart rate, catecholamine, plasma renin and aldosterone concentration, brain natriuretic peptide, urine liver-type fatty acid binding protein, and urinary albumin excretion ratio in the same patients by a cross-over design. Other biochemical parameters were also evaluated. Switching to cilnidipine did not change blood pressure but caused reduction in catecholamine concentrations in blood and urine and plasma aldosterone concentration, accompanied by significant reduction in brain natriuretic peptide, urine liver-type fatty acid binding protein, and albumin excretion ratio. These parameters other than brain natriuretic peptide were significantly increased after cilnidipine was changed to the original calcium channel blocker. In 33 hypertensive patients with type 2 diabetes mellitus, compared to other calcium channel blockers, cilnidipine suppressed sympathetic nerve activity and aldosterone, and significantly improved markers of cardiorenal disorders. Therefore, cilnidipine may be an important calcium channel blocker for use in combination with renin-angiotensin-aldosterone system inhibitors when dealing with hypertension complicated with diabetes mellitus. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  5. [Correlations between the coefficient of variation of RR intervals and sympathetic nerve activity following superior tilting in normotensive subjects and in patients with essential hypertension].

    Science.gov (United States)

    Shimazaki, M; Kikuchi, K; Yamaji, I; Kobayakawa, H; Yamamoto, M; Kudo, C; Wada, A; Mukai, H; Iimura, O

    1991-01-01

    The relationship between changes in sympathetic nerve activity and those in parasympathetic tone with a change in position was investigated in patients with essential hypertension using the coefficient of variation of RR intervals on electrocardiograms (CVRR). Mean arterial pressure (MAP), heart rate (HR), plasma noradrenaline concentration (pNA) and CVRR were measured in a supine position at rest and 20 min after having the head tilted 60 degrees superiorly in 10 normotensives (NT: 51.9 +/- 3.0 yrs) and 7 essential hypertensive patients (EHT: 51.0 +/- 2.8 yrs). After changing the position, CVRR decreased significantly in the NT, but not in the EHT; whereas, significant increases of both HR and pNA without significant changes in MAP were shown in both groups. A significant negative correlation between percentage changes in CVRR (% delta CVRR) and pNA (% delta pNA) were observed in the NT, but not in the EHT. However, there was no relationship of % delta CVRR to % delta MAP or to % delta HR in either group. It was suggested from the changes in CVRR that suppression of the parasympathetic tone, which occurs in the NT group corresponding to sympathetic augmentation to present a decrease in blood pressure with a change in position, may be impaired in the EHT group.

  6. Effect of pioglitazone on arterial baroreflex sensitivity and sympathetic nerve activity in patients with acute myocardial infarction and type 2 diabetes mellitus.

    Science.gov (United States)

    Yokoe, Hiroshi; Yuasa, Fumio; Yuyama, Reisuke; Murakawa, Kousuke; Miyasaka, Yoko; Yoshida, Susumu; Tsujimoto, Satoshi; Sugiura, Tetsuro; Iwasaka, Toshiji

    2012-06-01

    Pioglitazone has been shown to reduce the occurrence of fatal and nonfatal myocardial infarction (MI) in type 2 diabetes mellitus (DM). However, the mechanisms of such favorable effects remain speculative. The aim of this study was to investigate the effect of pioglitazone on arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA) in 30 DM patients with recent MI. Patients were randomly assigned to those taking pioglitazone (n = 15) and those not taking pioglitazone (n = 15) at 4 weeks after the onset of MI. BRS, MSNA, calculated homeostasis model assessment of insulin resistance index (HOMA-IR), and plasma adiponectin were measured at baseline and after 12 weeks. Pioglitazone increased plasma adiponectin (from 6.9 ± 3.3 μg/dL to 12.2 ± 7.1 μg/dL) and reduced HOMA-IR (from 4.0 ± 2.2 to 2.1 ± 0.9). In the pioglitazone group, MSNA decreased significantly (from 37 ± 7 bursts/min to 25 ± 8 bursts/min) and BRS increased significantly (from 6.7 ± 3.0 to 9.9 ± 3.2 ms/mm Hg) after 12 weeks. Furthermore, a significant relationship was found between the change in MSNA and HOMA-IR (r = 0.6, P = 0.042). Thus, pioglitazone decreased the sympathetic nerve traffic through the improvement of insulin resistance in DM patients with recent MI, which indicate that the sympathoinhibitory effects of pioglitazone may, at least in part, have contributed to the beneficial effects of pioglitazone.

  7. Renal denervation:history, today and tomorrow

    Institute of Scientific and Technical Information of China (English)

    BAO Ruo-tai; CHEN Zhong; MA Gen-shan

    2014-01-01

    Renal denervation is a new technique approved effective for resistant-hypertension treatment .The common renal denervation system consists of a generator and a flexible catheter .During this minimally invasive procedure , the interventionalist uses a steerable catheter with a radio frequency ( RF) energy electrode tip .The RF energy is delivered to the renal artery via standard femoral artery access .A series of 2-minute ablation are delivered in each renal artery to distroy the nerves system .The procedure does not involve a permanent device implant .By deactivating the renal nerves , and therefore reducing sympathetic nerve transmission , a significant and reliable reduction in blood pressure could be achieved .In this review, potential complications and future sights of renal denervation are also discussed .

  8. [Peripheral nerve disease associated with acute renal failure due to bromate poisoning].

    Science.gov (United States)

    Deshimaru, M; Miyagawa, T; Sumiyoshi, S; Nomura, Y

    1976-08-01

    A case of 21 year old male with neuropathy caused by renal insufficiency was present. He had taken bromate (mixed powder of potassium bromate and sodium bromate) for the purpose of suicide and suffered from acute renal insufficiency and hard of hearing. Renal dysfunction improved gradually by peritoneal dialysis and hemodialysis. However, on the 32th day after the onset, burning pain appeared in the bilateral feets. Following this, he began to complain of the disturbances of superficial and deep sensory below the ankle jerks and the weakness of his toes. Considering the clinical features, we supposed that the disturbance of the peripheral nerve was caused by uremia due to taking bromate. N. suralis was biopsied on the 80th day after the onset and examined electron microscopically. Electroscopical findings was as follows. Degeneration of the Schwann cells and irregularity or destruction of the myelin sheaths were observed. The axoplasm of the myelinated nerve fiber were relatively preserved as compared with the changes of the myelin sheaths. In the unmyelinated nerve fibers, cavity formations were observed. The findings of regeneration were not observed. From the electron microscopical findings, we speculate that the changes of the Schwann cells and the myelin sheaths are primary resulting from the disturbance of the metabolism of the Schwann cells. We speculate that anemia and hypoproteinemia caused by bromate disturbed regeneration.

  9. Inhibitory H3 receptors on sympathetic nerves of the pithed rat: activation by endogenous histamine and operation in spontaneously hypertensive rats.

    Science.gov (United States)

    Godlewski, G; Malinowska, B; Buczko, W; Schlicker, E

    1997-02-01

    Our previous results demonstrate the occurrence of presynaptic inhibitory histamine H3 receptors on sympathetic neurons innervating resistance vessels of the pithed rat. The present study, in which new H3 receptor ligands with increased potency and selectivity (imetit, clobenpropit) were used, was designed to further explore the role of H3 receptors in the regulation of the rat cardiovascular system. In particular we were interested whether these receptors may be activated by endogenous histamine and whether they are detectable in an experimental model of hypertension. All experiments were performed on pithed and vagotomized rats treated with rauwolscine 1 mumol/kg. In normotensive Wistar rats the electrical (1 Hz, 1 ms, 50 V for 20 s) stimulation of the preganglionic sympathetic nerve fibres increased diastolic blood pressure by about 35 mmHg. Two H3 receptor agonists, R-(-)-alpha-methylhistamine and imetit, inhibited the electrically induced increase in diastolic blood pressure in a dose-dependent manner. The maximal effect (about 25%) was obtained for R-(-)-alpha-methylhistamine at about 10 mumol/kg and for imetit at about 1 mumol/kg. Two H3 receptor antagonists, thioperamide 1 mumol/kg and clobenpropit 0.1 mumol/kg, attenuated the inhibitory effect of imetit. The neurogenic vasopressor response was increased by about 15% by thioperamide 1 mumol/kg and clobenpropit 0.1 mumol/kg and decreased by 25% by the histamine methyltransferase inhibitor metoprine 37 mumol/kg. R-(-)-alpha-Methylhistamine, imetit, thioperamide, clobenpropit and metoprine did not affect the vasopressor response to exogenously added noradrenaline 0.01 mumol/kg (which increased diastolic blood pressure by about 40 mmHg). Metoprine had only a very low affinity for H3 binding sites (labelled by 3H-N alpha-methylhistamine; pKi 4.46). In pithed Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats, electrical (1 Hz, 1 ms, 50 V for 10 s) stimulation increased diastolic blood pressure by 28

  10. 经导管消融选择性去肾交感神经治疗——未来心力衰竭治疗的热点%Catheter-based Selective Renal Artery Sympathetic Denervation-A Hot Spot of Managing Heart Failure in the Future

    Institute of Scientific and Technical Information of China (English)

    刘晓莉; 肖培林

    2013-01-01

    心力衰竭是各种心脏疾病的终末阶段.近几十年来,心力衰竭的治疗得到了一定的发展,但仍不能明显改善患者生存率,且需长期大量服药,严重影响患者生活质量.大量的研究显示:交感神经系统激活在心力衰竭的发生发展中扮演着重要角色.自上世纪40、50年代,学者们已开始进行去交感神经治疗心力衰竭的尝试,但碍于当时设备和技术的限制,治疗效果不尽人意.可喜的是,澳大利亚的权威学者近几年在美国心脏病学会/美国心脏协会心血管年会上介绍了一种安全、有效的新型去肾交感神经的方法,即经导管消融选择性去肾交感神经.该研究证实此方法可以明显降低全身交感活性.那么经导管消融去肾交感神经治疗能否成为未来心力衰竭治疗的热点呢?现将对去交感神经治疗心力衰竭的现状和进展做一综述.%Heart failure is the end-stage of serious heart disease. In recent decades, the heart failure treatment has gained some devel -opment, but still can' t significantly improve survival rate. The patients need to take a large amount of medication , and influence seriously the life quality of patients. Some study demonstrated that the somatic sympathetic nerves drive plays an important role in the development of heart failure. The sympathetic nerves denervation therapy has been researched since 1940 ~ 1950s, but the result is not satisfactory because of the restriction of poor technology. On the 2009 ACC/AHA cardiovascular annual conference , Krum MD introduced a new therapeutic method: the catheter-based renal artery ablation renal sympathetic nerves denervation . The HTN-2 Trail prove that the new method is safe and effective. The study (HTN-2) has been confirmed that the method can obviously reduce the whole body sympathetic activity . Will the catheter-based selective renal artery sympathetic denervation be a hot spot of managing heart failure in the future

  11. Diuresis and natriuresis caused by activation of VR1-positive sensory nerves in renal pelvis of rats.

    Science.gov (United States)

    Zhu, Yi; Wang, Youping; Wang, Donna H

    2005-10-01

    To test the hypothesis that activation of the vanilloid receptor 1 (VR1) expressed in sensory nerves innervating the renal pelvis leads to diuresis and natriuresis, a selective VR1 receptor agonist, capsaicin (2.4 nmol), or vehicle was perfused intravenously or into the left renal pelvis of anesthetized rats at a rate without changing renal perfusion pressure. Mean arterial pressure was not altered by capsaicin administered intravenously or into the renal pelvis. Capsaicin perfusion into the left renal pelvis but not intravenously caused significant increases in urine flow rate and urinary sodium excretion bilaterally in a dose-dependent manner, which were abolished by capsazepine, a selective VR1 receptor antagonist, given ipsilaterally to the renal pelvis or by ipsilateral renal denervation. Capsaicin given intravenously or into the left renal pelvis increased plasma calcitonin gene-related peptide levels to the same extent. Increased plasma calcitonin gene-related peptide levels induced by capsaicin (68.9+/-2.8 pg/mL) perfusion into the renal pelvis was prevented either by capsazepine (22.5+/-10.1 pg/mL) given ipsilaterally into the renal pelvis or by ipsilateral renal denervation (25.9+/-2.3 pg/mL). Taken together, our data show that unilateral activation of VR1-positive sensory nerves innervating the renal pelvis leads to bilateral diuresis and natriuresis via a mechanism that is independent of plasma calcitonin gene-related peptide levels. These data suggest that VR1-positive sensory nerves in the kidney enhance renal excretory function, a mechanism that may be critically involved in sodium and fluid homeostasis.

  12. Sympathetic Nerve Activity Maintains an Anti-Inflammatory State in Adipose Tissue in Male Mice by Inhibiting TNF-α Gene Expression in Macrophages.

    Science.gov (United States)

    Tang, Lijun; Okamoto, Shiki; Shiuchi, Tetsuya; Toda, Chitoku; Takagi, Kazuyo; Sato, Tatsuya; Saito, Kumiko; Yokota, Shigefumi; Minokoshi, Yasuhiko

    2015-10-01

    Adipose tissue macrophages (ATMs) play an important role in the inflammatory response in obese animals. How ATMs are regulated in lean animals has remained elusive, however. We now show that the sympathetic nervous system (SNS) is necessary to maintain the abundance of the mRNA for the proinflammatory cytokine TNF-α at a low level in ATMs of lean mice. Intracerebroventricular injection of agouti-related neuropeptide increased the amount of TNF-α mRNA in epididymal (epi) white adipose tissue (WAT), but not in interscapular brown adipose tissue (BAT), through inhibition of sympathetic nerve activity in epiWAT. The surgical denervation and β-adrenergic antagonist propranolol up-regulated TNF-α mRNA in both epiWAT and BAT in vivo. Signaling by the β2-adrenergic receptor (AR) and protein kinase A down-regulated TNF-α mRNA in epiWAT explants and suppressed lipopolysaccharide-induced up-regulation of TNF-α mRNA in the stromal vascular fraction of this tissue. β-AR-deficient (β-less) mice manifested an increased plasma TNF-α concentration and increased TNF-α mRNA abundance in epiWAT and BAT. TNF-α mRNA abundance was greater in ATMs (CD11b(+) cells of the stromal vascular fraction) from epiWAT or BAT of wild-type mice than in corresponding CD11b(-) cells, and β2-AR mRNA abundance was greater in ATMs than in CD11b(-) cells of epiWAT. Our results show that the SNS and β2-AR-protein kinase A pathway maintain an anti-inflammatory state in ATMs of lean mice in vivo, and that the brain melanocortin pathway plays a role in maintaining this state in WAT of lean mice via the SNS.

  13. Sympathetic nerve activity in normal and cystic follicles from isolated bovine ovary: local effect of beta-adrenergic stimulation on steroid secretion

    Directory of Open Access Journals (Sweden)

    Ortega Hugo H

    2011-05-01

    Full Text Available Abstract Cystic ovarian disease (COD is an important cause of abnormal estrous behavior and infertility in dairy cows. COD is mainly observed in high-yielding dairy cows during the first months post-partum, a period of high stress. We have previously reported that, in lower mammals, stress induces a cystic condition similar to the polycystic ovary syndrome in humans and that stress is a definitive component in the human pathology. To know if COD in cows is also associated with high sympathetic activity, we studied isolated small antral (5mm, preovulatory (10mm and cystic follicles (25mm. Cystic follicles which present an area 600 fold greater compared with preovulatory follicles has only 10 times less concentration of NE as compared with small antral and preovulatory follicles but they had 10 times more NE in follicular fluid, suggesting a high efflux of neurotransmitter from the cyst wall. This suggestion was reinforced by the high basal release of recently taken-up 3H-NE found in cystic follicles. While lower levels of beta-adrenergic receptor were found in cystic follicles, there was a heightened response to the beta-adrenergic agonist isoproterenol and to hCG, as measured by testosterone secretion. There was however an unexpected capacity of the ovary in vitro to produce cortisol and to secrete it in response to hCG but not to isoproterenol. These data suggest that, during COD, the bovine ovary is under high sympathetic nerve activity that in addition to an increased response to hCG in cortisol secretion could participate in COD development.

  14. The human sympathetic nervous system: its relevance in hypertension and heart failure.

    Science.gov (United States)

    Parati, Gianfranco; Esler, Murray

    2012-05-01

    Evidence assembled in this review indicates that sympathetic nervous system dysfunction is crucial in the development of heart failure and essential hypertension. This takes the form of persistent and adverse activation of sympathetic outflows to the heart and kidneys in both conditions. An important goal for clinical scientists is translation of the knowledge of pathophysiology, such as this, into better treatment for patients. The achievement of this 'mechanisms to management' transition is at different stages of development with regard to the two disorders. Clinical translation is mature in cardiac failure, knowledge of cardiac neural pathophysiology having led to the introduction of beta-adrenergic blockers, an effective therapy. With essential hypertension perhaps we are on the cusp of effective translation, with recent successful testing of selective catheter-based renal sympathetic nerve ablation in patients with resistant hypertension, an intervention firmly based on the demonstration of activation of the renal sympathetic outflow. Additional evidence in this regard is provided by the results of pilot studies exploring the possibility to reduce blood pressure in resistant hypertensives through electrical stimulation of the area of carotid baroreceptors. Despite the general importance of the sympathetic nervous system in blood pressure regulation, and the specific demonstration that the blood pressure elevation in essential hypertension is commonly initiated and sustained by sympathetic nervous activation, drugs antagonizing this system are currently underutilized in the care of patients with hypertension. Use of beta-adrenergic blocking drugs is waning, given the propensity of this drug class to have adverse metabolic effects, including predisposition to diabetes development. The blood pressure lowering achieved with carotid baroreceptor stimulation and with the renal denervation device affirms the importance of the sympathetic nervous system in

  15. Stress and Female Reproductive System: Disruption of Corticotropin-Releasing Hormone/Opiate Balance by Sympathetic Nerve Traffic

    Directory of Open Access Journals (Sweden)

    Farideh Zafari Zangeneh

    2009-09-01

    Full Text Available Nowadays stress is an integral part of everyday living and the physiological and behavioral consequences of exposure to stressful situations have been extensively studied for decades. The stress response is a necessary mechanism but disrupts homeostatic process and it is sub served by a complex system located in both the central nervous system (CNS and the periphery. Stressor-induced activation of the hypothalamus–pituitary–adrenal (HPA axis and the sympathetic nervous system (SNS results in a series of neural and endocrine adaptations known as the "stress response" or "stress cascade." The stress cascade is responsible for allowing the body to make the necessary physiological and metabolic changes required to cope with the demands of a homeostatic challenge. Normal activation of the HPA axis is essential for reproduction, growth, metabolic homeostasis, and responses to stress and they are critical for adapting to changes in the external environment. The regulation of gonadal function in men and women is under the control of the HPA. This regulation is complex and sex steroids are important regulators of GnRH and gonadotropin release through classical feedback mechanisms in the hypothalamus and the pituitary. The present overview focuses on the neuroendocrine infrastructure of the adaptive response to stress and its effects on the female reproductive system. 

  16. Renal sympathetic denervation as an adjunct to catheter ablation for the treatment of ventricular electrical storm in the setting of acute myocardial infarction.

    Science.gov (United States)

    Hoffmann, Boris A; Steven, Daniel; Willems, Stephan; Sydow, Karsten

    2013-10-01

    We present a case of ventricular storm (VS) in a patient with acute ST-elevation myocardial infarction (STEMI). After initial successful thrombus extraction and percutaneous coronary intervention (PCI) of the proximal left anterior descending (LAD) coronary artery, a 63-year-old male patient showed recurrent monomorphic ventricular tachycardia (VT) and fibrillation (VF) episodes refractory to antiarrhythmic drug therapy. After initial successful VT ablation, fast VT and VF episodes remained an evident problem despite maximum antiarrhythmic drug therapy. Due to an increasing instability, renal sympathetic denervation (RDN) was performed. ICD interrogation and 24-hour Holter monitoring excluded recurrent episodes of VT or VF at a 6-month follow-up (FU) after discharge. This case highlights that RDN was effective and safely performed in a hemodynamically unstable patient with VS after STEMI and adjunct catheter ablation. RDN may open a new avenue for an adjunctive interventional bailout treatment of such highly challenging patients.

  17. Effects of renal sympathetic denervation on exercise blood pressure, heart rate, and capacity in patients with resistant hypertension.

    Science.gov (United States)

    Ewen, Sebastian; Mahfoud, Felix; Linz, Dominik; Pöss, Janine; Cremers, Bodo; Kindermann, Ingrid; Laufs, Ulrich; Ukena, Christian; Böhm, Michael

    2014-04-01

    Renal denervation reduces office blood pressure in patients with resistant hypertension. This study investigated the effects of renal denervation on blood pressure, heart rate, and chronotropic index at rest, during exercise, and at recovery in 60 patients (renal denervation group=50, control group=10) with resistant hypertension using a standardized bicycle exercise test protocol performed 6 and 12 months after renal denervation. After renal denervation, exercise blood pressure at rest was reduced from 158±3/90±2 to 141±3/84±4 mm Hg (PExercise blood pressure tended to be lower at all stages of exercise at 6- and 12-month follow-up in patients undergoing renal denervation, although reaching statistical significance only at mild-to-moderate exercise levels (75-100 W). At recovery after 1 minute, blood pressure decreased from 201±4/95±2 to 177±4/88±2 (PHeart rate was reduced after renal denervation from 71±3 bpm at rest, 128±5 bpm at maximum workload, and 96±5 bpm at recovery after 1 minute to 66±2 (Pexercise time increased from 6.59±0.33 to 8.4±0.32 (Pheart rate during exercise, improved mean workload, and increased exercise time without impairing chronotropic competence.

  18. Effect of chronic renal failure, dialysis and transplantation on motor nerve conduction velocity in children.

    Science.gov (United States)

    Arbus, G. S.; Barnor, N. A.; Hsu, A. C.; Murphy, E. G.; Radde, I. C.

    1975-01-01

    Ulnar and peroneal motor nerve conduction volocities (MNCVs) were measured in 47 children in a dialysis-transplantation program. Mean peroneal MNCV was significantly decreased from normal in children with mild renal failure (serum creatinine concentration, 1.5 to 2.9 mg/dl), whereas ulnar MNCV was significantly decreased only when the serum creatinine value was at least 9 mg/dl. Both ulnar and peroneal MNCVs remained unchanged during long-term hemodialysis or peritoneal dialysis; however, after individual dialyses ulnar MNCV increased. After renal transplantation ulnar MNCV returned to normal within a year and peroneal MNCV within 3 years. Before dialysis was required and during long-term dialysis most plasma magnesium values were elevated; ionized calcium activity was decreased in about 50% of determinations. After transplantation and the concentration of divalent cations rapidly returned to normal. These children differed from adults studied in that (a) there was no correlation between severity of renal failure and MNCV, (b) long-term dialysis did not improve MNCV and (c) peroneal velocities did not recover for 3 years after transplantation. PMID:1098759

  19. Regulation of N- and L-type Ca2+ channels in adult frog sympathetic ganglion B cells by nerve growth factor in vitro and in vivo.

    Science.gov (United States)

    Lei, S; Dryden, W F; Smith, P A

    1997-12-01

    To examine mechanisms responsible for the long-term regulation of Ca2+-channels in an adult neuron, changes in whole cell Ba2+ current (IBa) were examined in adult bullfrog sympathetic ganglion B cells in vitro. Cells were cultured at low density in defined, serum free medium. After 15 days, total IBa was similar to the initial value, whereas IBa density was reduced by approximately 36%, presumably due to an increase in neuronal surface area. By contrast, IBa density remained constant after 6-15 days in the presence of murine beta-NGF (200 ng/ml), and total IBa was almost doubled. Inclusion of cytosine arabinoside (Ara-C; 10 microM) to inhibit proliferation of nonneuronal cells, did not affect the survival of neurons in the absence of nerve growth factor (NGF) nor did it attenuate IBa. Ara-C did not prevent the effect of NGF on IBa. There were three independent components to the action of NGF; during 6-9 days, it increased omega-conotoxin-GVIA-sensitive N-type IBa (IBa,N); increased nifedipine-sensitive L-type IBa (IBa,L) and decreased inactivation of the total Ba2+ conductance (gBa). The latter effect involved a selective decrease in the amplitude of one of the four kinetic components that describe the inactivation process. Total IBa was also 55.8% larger than control in the somata of B cells acutely dissociated from leopard frogs that had received prior subcutaneous injections of NGF. By contrast, injection of NGF antiserum decreased total IBa by 29.4%. There was less inactivation of gBa in B cells from NGF-injected animals than in cells from animals injected with NGF antiserum (P < 0.001). These data suggest that NGF-like molecule(s) play(s) a role in the maintenance of IBa in an adult amphibian sympathetic neuron; the presence of NGF may allow the neuron to maintain a constant relationship between cell size and current density. They also show that IBa inactivation in an adult neuron can be modulated in a physiologically relevant way by an extracellular ligand.

  20. Renal denervation: a new therapeutic approach for resistant hypertension

    Institute of Scientific and Technical Information of China (English)

    Cao Longxing; Fu Qiang; Wang Binghui; Li Zhiliang

    2014-01-01

    Objective To review the advances in studies on renal denervation.Data sources References concerning renal denervation and resistant hypertension cited in this review were collected from PubMed published in English and those of renal denervation devices from official websites of device manufacturers up to January 2014.Study selection Articles with keywords "renal denervation" and "resistant hypertension" were selected.Results Renal and systemic sympathetic overactivity plays an important role in pathology of hypertension as well as other diseases characterized by sympathetic overactivity.Renal denervation is a new,catheter based procedure to reduce renal and systemic sympathetic overactivity by disruption of renal sympathetic efferent and afferent nerves through radiofrequency or ultrasound energy delivered to the endoluminal surface of both renal arteries.Although several studies have shown the efficacy and safety of renal denervation in the treatment of resistant hypertension and the potential benefit of the procedure in other diseases,Symplicity HTN 3 study,the most rigorous clinical trial of renal denervation to date,failed to meet its primary endpoint.The procedure also has other limitations such as the lack of long term,efficacy and safety data and the lack of the predictors for the blood pressure lowering response and nonresponse to the procedure.An overview of current renal denervation devices holding Conformité Européenne mark is also included in this review.Conclusions Renal denervation is a promising therapeutic approach in the management of resistant hypertension and other diseases characterized by sympathetic overactivity.In its early stage of clinical application,the efficacy of the procedure is still controversial.Large scale,blind,randomized,controlled clinical trials are still necessary to address the limitations of the procedure.

  1. Sympathetic hyperactivity in patients with chronic kidney disease

    NARCIS (Netherlands)

    Neumann, N.

    2007-01-01

    Sympathetic hyperactivity in patients with chronic kidney disease Chronic kidney disease (CKD) is often characterized by the presence of sympathetic hyperactivity. This contributes to the pathogenesis of renal hypertension. It is also associated with cardiovascular (CV) morbidity and mortality indep

  2. Number of ablated spots in the course of renal sympathetic denervation in CKD patients with uncontrolled hypertension: EnligHTN vs. Standard irrigated cardiac ablation catheter.

    Science.gov (United States)

    Kiuchi, M G; Chen, S; Rodrigues Paz, L M; Pürerfellner, H

    2017-08-04

    Hypertension was both a mutual cause and the main concern of chronic kidney disease (CKD). Blood pressure control is more problematic in the company of CKD. This study compares the effects of renal sympathetic denervation (RSD) on 24-h ambulatory blood pressure measurements (ABPM) and renal function in individuals with CKD and uncontrolled hypertension by unlike a number of ablated spots using the EnligHTN catheter and the standard irrigated cardiac ablation catheter (SICAC), Flexability. The 112 subjects were randomly divided into two groups according to the catheter that would be used in the procedure EnligHTN (n=56) or Flexability (n=56). Into each group, we created 5 subgroups according to the number of ablated spots: 4, 8, 12, 16 and 20. All of them were followed for exactly 6 months to assess all the parameters measured in this investigation. Comparing the Δ 24-h systolic ABPM according to the number of ablated spots 4 and 20 for EnligHTN vs. Flexability, respectively, the differences were: -3.6±0.9 vs. -6.3±1.4mmHg (Prenal function in both groups. These effects were more marked and important in subgroups underwent a great number of ablated spots using the SICAC. Copyright © 2017 SEH-LELHA. Publicado por Elsevier España, S.L.U. All rights reserved.

  3. Gender differences in sympathetic nervous system regulation.

    Science.gov (United States)

    Hinojosa-Laborde, C; Chapa, I; Lange, D; Haywood, J R

    1999-02-01

    1. Females are protected against the development of hypertension. The purpose of the current review is to present the evidence for gender differences in the regulation of the sympatho-adrenal nervous system and to determine if these differences support the hypothesis that, in females, the regulation of the sympathetic nervous system (SNS) is altered such that sympatho-adrenal activation is attenuated or sympatho-adrenal inhibition is augmented. 2. The central control of sympatho-adrenal function is different in females and responses vary during the oestral and menstrual cycles. Pathways regulating the SNS appear to be less sensitive to excitatory stimuli and more sensitive to inhibitory stimuli in females compared with males. 3. Gender differences in arterial baroreflex sensitivity suggest that females may have a greater baroreflex sensitivity, such that alterations in blood pressure are more efficiently controlled than in males. Cardiopulmonary reflex inhibition of sympathetic nerve activity is greater in females, possibly resulting in a greater renal excretory function. 4. An attenuated sensitivity to adrenergic nerve stimulation, but not to noradrenaline (NA), suggests that gender differences in noradrenergic neurotransmission may protect females against sympathetic hyperactivity. Gender differences in the regulation of NA release via presynaptic alpha 2-adrenoceptors, the vasoconstrictor response to the cotransmitter neuropeptide Y and the clearance of catecholamines are consistent with this hypothesis. 5. Similarly, attenuated stress-induced increases in plasma catecholamines in women suggest that females are less sensitive and/or less responsive to adrenal medullary activation. This is supported by findings of gender differences in adrenal medullary catecholamine content, release and degradation. 6. We conclude that there is strong evidence that supports the hypothesis that, in females, the regulation of the SNS is altered such that sympatho

  4. Changes of norepinephrine and tumor necrosis factor in submandibular gland of rats with sympathetic nerve injury and the protective effect of 17 beta-estradiol

    Institute of Scientific and Technical Information of China (English)

    Yagao Feng; Suya Deng; Zhenqi Liu; Min Hu; Houjun Yan; Qiusheng Wang

    2006-01-01

    BACKGROUND: Recent researches have indicated that estrogen has extensive neuroprotective effects. So some studies designed ovariectomized animal models and administrated with estrogen, so as to verify its neuroprotective effects.OBJECTIVE: To observe the effect of 17 beta-estradiol on the content of norepinephrine (NE) and level of tumor necrosis factor (TNF) in submandibular glands of rats with sympathetic nerve injury, and analyze the dose-dependence and pathway of action.DESIGN: A randomized control animal study.SETTINGS: Department of Hand Surgery, the 252 Hospital of Chinese PLA; Department of Hand Surgery,Union Hospital affiliated to Tongji Medical College, Huazhong University of Science and Technology.MATERIALS: Fifty healthy female Wistar rats were randomly divided into 5 groups with 10 rats in each group: sham-operated group, ovariectomy+6-OHDA+saline group, ovariectomy+6-OHDA+17β-estradiol 50,200 and 500 μg/kg groups.METHODS: The experiments were carried out in Tongji Medical College, Huazhong University of Science and Technology between October 2005 and March 2006. Bilateral ovaries were only exposed but not resected for the rats in the sham-operated group, but bilateral ovaries were resected in all the other groups. In the ovariectomy+6-OHDA+17β-estradiol 50, 200 and 500 μg/kg groups, the rats were administrated with intraperitoneal injection of 6-OHDA (8 mg/kg), and then immediately given 17β-estradiol of corresponding dosages respectively, once a day for 10 days continuously. Rats in the sham-operated group and ovariectomy+6-OHDA+saline group were administrated with saline of the same volume. After administration, 5 rats in each group were killed to determine the NE contents in bilateral submandibular glands with high performance liquid chromatography-electrochemical detector (HPLC-ECD), and the other 5 rats were used to determine the TNF levels in submandibular glands with enzyme-linked immunosorbant assay.MATN OUTCOME MEASURES: The NE contents

  5. The addition of renal sympathetic denervation to pulmonary vein isolation reduces recurrence of paroxysmal atrial fibrillation in chronic kidney disease patients.

    Science.gov (United States)

    Kiuchi, Márcio Galindo; Chen, Shaojie; E Silva, Gustavo Ramalho; Rodrigues Paz, Luis Marcelo; Kiuchi, Tetsuaki; de Paula Filho, Ary Getulio; Lima Souto, Gladyston Luiz

    2017-03-01

    Atrial fibrillation (AF) frequently complicates chronic kidney disease (CKD). AF treatment is challenging and requires complete pulmonary vein isolation (PVI). Recently, renal sympathetic denervation (RSD) has been reported to reduce AF recurrence when performed alongside PVI. A prospective therapeutic study of patients with controlled hypertension and paroxysmal AF was undertaken. Renal function was evaluated using estimated glomerular filtration rate. Outcomes for patients with normal renal function who underwent PVI (n = 101) were compared with those for CKD patients who underwent either PVI alone (n = 96) or PVI + RSD (n = 39). The primary endpoint was recurrence of AF recorded by 24-h Holter monitoring. During the 22.4 ± 12.1 months following intervention, the incidence of AF recurrence was higher in CKD patients treated with PVI alone (61.5 %) than in CKD patients treated with PVI + RSD (38.5 %; HR 1.86, 95 % CI 1.14-3.03, P = 0.0251) or patients without CKD subjected to PVI (35.6 %; hazard ratio (HR) 2.27, 95 % confidence interval (CI) 1.51-3.42, P PVI significantly reduced AF recurrence in CKD stage 4, but not stage 2 or 3, patients. Ambulatory blood pressure and mean heart rate were not different between groups or time points. No complications of either procedure were observed. PVI + RSD is a safe treatment that is superior to PVI alone for treatment of paroxysmal AF in CKD patients.

  6. Pulmonary vein isolation alone and combined with renal sympathetic denervation in chronic kidney disease patients with refractory atrial fibrillation

    Directory of Open Access Journals (Sweden)

    Márcio G. Kiuchi

    2016-12-01

    Conclusion: PVI + RSD were associated with a lower AF recurrence rate than PVI alone; it also improved renal function and some echocardiographic parameters. These encouraging data will serve as baseline information for further long-term studies on larger patient populations.

  7. The oestrogenized rat myometrium inhibits organotypic sympathetic reinnervation.

    Science.gov (United States)

    Brauer, M M; Chávez-Genaro, R; Richeri, A; Viettro, L; Frias, A I; Burnstock, G; Cowen, T

    2002-10-31

    Chronic administration of oestrogen to rats during the infantile/prepubertal period provokes, at 28 days of age, complete loss of noradrenaline-labelled intrauterine sympathetic nerves. It is not known whether oestrogen inhibits the growth or causes the degeneration of developing uterine sympathetic nerves, or whether the uterus recovers its innervation following cessation of infantile/prepubertal oestrogen treatment. In the present study, we analysed the time-course of the effects of oestrogen on the development of uterine sympathetic nerves in the rat, using histochemical methods. In addition, the pattern of sympathetic reinnervation of the uterus of intact and ovariectomised females was assessed 3 and 6 months after cessation of chronic oestrogen treatment. The ability of sympathetic nerves to reinnervate the oestrogenized uterine tissue was assessed in intraocular transplants of uterine myometrium into ovariectomised host rats. Early exposure to oestrogen did not inhibit the approach of sympathetic nerves to the uterus, but prevented the normal growth and maturation of intrauterine sympathetic fibres and abolished the innervation that reached the organ before initiation of treatment. Three or six months following cessation of oestrogen treatment, most of the sympathetic nerves were restricted to the mesometrium and mesometrial entrance, whereas intrauterine innervation remained persistently depressed as a consequence of a sustained oestrous-like state provoked by ovarian dysfunction (polycystic ovary). An organotypic regrowth of uterine sympathetic nerves was observed in ovariectomised infantile/prepubertal oestrogen-treated animals. After 5 weeks in oculo, the innervation of oestrogenized myometrial transplants was reduced by 50%, and substantial changes in the pattern of reinnervation were observed. In control transplants, 86% of the nerves were terminal varicose myometrial and perivascular nerve fibres, whereas 14% were preterminal nerve bundles. In

  8. 颈总动脉交感神经网剥脱术治疗脑性瘫痪的探讨%Discussion of common carotid artery sympathetic nerve net exfoliation therapy treating cerebral palsy

    Institute of Scientific and Technical Information of China (English)

    尹彪中; 李如求; 成顺成

    2002-01-01

    Objective To discuss mechanism of common carotid artery sympathetic nerve net exfoliation therapy treating sequela of cerebral palsy. Methods Examing and assessing before and after operation, curative effect analysis, Wals value assay and 1 year follow up to 124 patients. Result Score of patients in this group reached excellent 1 week after operation, reached good 1 year after operation, Wals value measure P≤ 0.05. Conclusion This operation had an effect on the promotion of mixed type; athetosis type cerebral palsy, upper limb function disorder and malfunction.

  9. Subfornical organ mediates sympathetic and hemodynamic responses to blood-borne proinflammatory cytokines.

    Science.gov (United States)

    Wei, Shun-Guang; Zhang, Zhi-Hua; Beltz, Terry G; Yu, Yang; Johnson, Alan Kim; Felder, Robert B

    2013-07-01

    Proinflammatory cytokines play an important role in regulating autonomic and cardiovascular function in hypertension and heart failure. Peripherally administered proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), act on the brain to increase blood pressure, heart rate, and sympathetic nerve activity. These molecules are too large to penetrate the blood-brain barrier, and so the mechanisms by which they elicit these responses remain unknown. We tested the hypothesis that the subfornical organ (SFO), a forebrain circumventricular organ that lacks a blood-brain barrier, plays a major role in mediating the sympathetic and hemodynamic responses to circulating proinflammatory cytokines. Intracarotid artery injection of TNF-α (200 ng) or IL-1β (200 ng) dramatically increased mean blood pressure, heart rate, and renal sympathetic nerve activity in rats with sham lesions of the SFO (SFO-s). These excitatory responses to intracarotid artery TNF-α and IL-1β were significantly attenuated in SFO-lesioned (SFO-x) rats. Similarly, the increases in mean blood pressure, heart rate, and renal sympathetic nerve activity in response to intravenous injections of TNF-α (500 ng) or IL-1β (500 ng) in SFO-s rats were significantly reduced in the SFO-x rats. Immunofluorescent staining revealed a dense distribution of the p55 TNF-α receptor and the IL-1 receptor accessory protein, a subunit of the IL-1 receptor, in the SFO. These data suggest that SFO is a predominant site in the brain at which circulating proinflammatory cytokines act to elicit cardiovascular and sympathetic responses.

  10. Effects of adding intravenous nicorandil to standard therapy on cardiac sympathetic nerve activity and myocyte dysfunction in patients with acute decompensated heart failure

    Energy Technology Data Exchange (ETDEWEB)

    Kasama, Shu [Gunma University Graduate School of Medicine, Department of Medicine and Biological Science (Cardiovascular Medicine), Maebashi, Gunma (Japan); Cardiovascular Hospital of Central Japan (Kitakanto Cardiovascular Hospital), Department of Cardiovascular Medicine, Gunma (Japan); Toyama, Takuji; Funada, Ryuichi; Takama, Noriaki; Koitabashi, Norimichi; Kurabayashi, Masahiko [Gunma University Graduate School of Medicine, Department of Medicine and Biological Science (Cardiovascular Medicine), Maebashi, Gunma (Japan); Ichikawa, Shuichi [Cardiovascular Hospital of Central Japan (Kitakanto Cardiovascular Hospital), Department of Cardiovascular Medicine, Gunma (Japan); Suzuki, Yasuyuki; Matsumoto, Naoya [Nihon University School of Medicine, Department of Cardiology, Tokyo (Japan); Sato, Yuichi [Health Park Clinic, Department of Imaging, Takasaki, Gunma (Japan)

    2015-04-01

    Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, improves cardiac sympathetic nerve activity (CSNA) in ischemic heart disease or chronic heart failure. However, its effects on CSNA and myocyte dysfunction in acute heart failure (AHF) remain unclear. We investigated the effects of adding intravenous nicorandil to standard therapy on CSNA and myocyte dysfunction in AHF. We selected 70 patients with mild to moderate nonischemic AHF who were treated with standard conventional therapy soon after admission. Thirty-five patients were assigned to additionally receive intravenous nicorandil (4-12 mg/h; group A), whereas the remaining patients continued their current drug regimen (group B). Delayed total defect score (TDS), delayed heart to mediastinum count (H/M) ratio, and washout rate (WR) were determined by {sup 123}I-metaiodobenzylguanidine (MIBG) scintigraphy within 3 days of admission and 4 weeks later. High sensitivity troponin T (hs-TnT) level was also measured at the same time points. After treatment, MIBG scintigraphic parameters significantly improved in both groups. However, the extent of the changes in these parameters in group A significantly exceeded the extent of the changes in group B [TDS -11.3 ± 4.3 in group A vs -4.0 ± 6.0 in group B (p < 0.01); H/M ratio 0.31 ± 0.16 vs 0.14 ± 0.16 (p < 0.01); WR -13.8 ± 7.8 % vs -6.1 ± 8.9 % (p < 0.01)]. The hs-TnT level decreased significantly from 0.052 ± 0.043 to 0.041 ± 0.033 ng/ml (p < 0.05) in group A, but showed no significant change in group B. Moreover, in both groups, no relationships between the extent of changes in MIBG parameters and hs-TnT level were observed. Adding intravenous nicorandil to standard therapy provides additional benefits for CSNA and myocyte dysfunction over conventional therapy alone in AHF patients. Furthermore, the mechanisms of improvement in CSNA and myocyte dysfunction after nicorandil treatment in AHF patients were distinct. (orig.)

  11. Organ-specific activation of the gastric branch of the efferent vagus nerve by ghrelin in urethane-anesthetized rats.

    Science.gov (United States)

    Habara, Hiromi; Hayashi, Yujiro; Inomata, Norio; Niijima, Akira; Kangawa, Kenji

    2014-01-01

    Ghrelin plays multiple physiological roles such as growth hormone secretion and exerting orexigenic actions; however, its physiological roles in the electrical activity of autonomic nerves remain unclear. Here, we investigated the effects of human ghrelin on several autonomic nerve activities in urethane-anesthetized rats using an electrophysiological method. Intravenous injection of ghrelin at 3 μg/kg significantly and transiently potentiated the efferent activity of the gastric vagus nerve; however, it did not affect the efferent activity of the hepatic vagus nerve. The activated response to ghrelin in the gastric efferent vagus nerve was not affected by the gastric afferent vagotomy, suggesting that this effect was not induced via the gastric afferent vagus nerve. Ghrelin did not affect the efferent activity of the brown adipose tissue, adrenal gland sympathetic nerve, and the renal sympathetic nerve. In addition, rectal temperature and the plasma concentrations of norepinephrine, corticosterone, and renin were also not changed by ghrelin. These findings demonstrate that ghrelin stimulates the gastric efferent vagus nerve in an organ-specific manner without affecting the gastric afferent vagus nerve and that ghrelin does not acutely affect the efferent basal activity of the sympathetic nerve in rats.

  12. Renal sympathetic denervation in patients with treatment-resistant hypertension after witnessed intake of medication before qualifying ambulatory blood pressure.

    Science.gov (United States)

    Fadl Elmula, Fadl Elmula Mohamed; Hoffmann, Pavel; Fossum, Eigil; Brekke, Magne; Gjønnæss, Eyvind; Hjørnholm, Ulla; Kjær, Vibeke N; Rostrup, Morten; Kjeldsen, Sverre E; Os, Ingrid; Stenehjem, Aud-E; Høieggen, Aud

    2013-09-01

    It is unknown whether the decline in blood pressure (BP) after renal denervation (RDN) is caused by denervation itself or concomitantly improved drug adherence. We aimed to investigate the BP lowering effect of RDN in true treatment-resistant hypertension by excluding patients with poor drug adherence. Patients with resistant hypertension (n=18) were referred for a thorough clinical and laboratory work-up. Treatment-resistant hypertension was defined as office systolic BP>140 mm Hg, despite maximally tolerated doses of ≥ 3 antihypertensive drugs, including a diuretic. In addition, ambulatory daytime systolic BP>135 mm Hg was required after witnessed intake of antihypertensive drugs to qualify. RDN (n=6) was performed with Symplicity Catheter System. The mean office and ambulatory BPs remained unchanged at 1, 3, and 6 months in the 6 patients, whereas there was no known change in antihypertensive medication. Two patients, however, had a fall in both office and ambulatory BPs. Our findings question whether BP falls in response to RDN in patients with true treatment-resistant hypertension. Additional research must aim to verify potential BP lowering effect and identify a priori responders to RDN before this invasive method can routinely be applied to patients with drug-resistant hypertension. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT01673516.

  13. Renal denervation for treatment of cardiac arrhythmias: state of the art and future directions.

    Science.gov (United States)

    Kosiuk, Jedrzej; Hilbert, Sebastian; Pokushalov, Evgeny; Hindricks, Gerhard; Steinberg, Jonathan S; Bollmann, Andreas

    2015-02-01

    It has now been more than a quarter of a century since modulation of the sympathetic nervous system was proposed for the treatment of cardiac arrhythmias of different origins. But it has also been some time since some of the early surgical attempts have been abandoned. With the development of ablation techniques, however, new approaches and targets have been recently introduced that have revolutionized our way of thinking about sympathetic modulation. Renal nerve ablation technology is now being successfully used for the treatment of resistant hypertension, but the indication spectrum might broaden and new therapeutic options might arise in the near future. This review focuses on the possible impact of renal sympathetic system modulation on cardiac arrhythmias, the current evidence supporting this approach, and the ongoing trials of this method in electrophysiological laboratories. We will discuss the potential roles that sympathetic modulation may play in the future.

  14. How does renal denervation lower blood pressure and when should this technique be considered for the treatment of hypertension?

    Science.gov (United States)

    Leong, Kui Toh Gerard; Krum, Henry

    2013-11-01

    Resistant hypertension poses significant health concerns. There are strong demands for new safe therapeutics to control resistant hypertension, while addressing its common causes, specifically poor compliance to lifelong polypharmacy, lifestyle modification and physician inertia. The sympathetic nervous system plays a significant pathophysiological role in hypertension. Surgical sympathectomy for blood pressure reduction is an old but extremely efficacious therapeutic concept, since abandoned, with the dawn of safer contemporary pharmacology era. Recently, clinical studies have revealed promising results for safe and sustained blood pressure reduction with percutaneous renal sympathetic denervation. This is a novel, minimally-invasive, device-based therapy, specifically targeting and ablating the renal artery nerves with radiofrequency waves, without permanent implantation. There are also reported additional benefits in related comorbidities, such as impaired glucose metabolism, renal impairment, left ventricular hypertrophy, heart failure, and others. This review will focus on how selective renal sympathetic denervation works, as well as its present and potential therapeutic indications.

  15. Local Sympathetic Denervation of Femoral Artery in a Rabbit Model by Using 6-Hydroxydopamine In Situ

    Directory of Open Access Journals (Sweden)

    Yufei Jin

    2014-01-01

    Full Text Available Both artery bundle and sympathetic nerve were involved with the metabolism of bone tissues. Whether the enhancing effects of artery bundle result from its accompanying sympathetic nerve or blood supply is still unknown. There is no ideal sympathetic nerve-inhibited method for the in situ denervation of artery bundle. Therefore, we dipped the femoral artery in the 6-hydroxydopamine (6-OHDA locally and observed its effect. Compared with control group, the in situ treatment of 6-OHDA did not damage the normal structure of vascular bundle indicated by hematoxylin-eosin (HE staining. However, the functions of sympathetic nerve was completely inhibited for more than 2 weeks, and only a few function of sympathetic nerve resumed 4 weeks later, evidenced by glyoxylic acid staining and the expression of tyrosine hydroxylase (TH and nerve peptide Y (NPY. Thus, 6-OHDA is promising as an ideal reagent for the local denervation of sympathetic nerve from artery system.

  16. Is baroreflex control of sympathetic activity and heart rate active in the preterm fetal sheep?

    Science.gov (United States)

    Booth, Lindsea C; Malpas, Simon C; Barrett, Carolyn J; Guild, Sarah-Jane; Gunn, Alistair J; Bennet, Laura

    2009-03-01

    The arterial baroreflex is a fundamental reflex that buffers rapid changes in arterial blood pressure (BP) via regulation of the heart rate and sympathetic nerve activity to the vasculature. In adults a sigmoidal relationship between BP and both heart rate and sympathetic nerve activity is well documented. Its role in blood pressure control before birth is unclear. Preterm babies have a high incidence of low BP, especially in the first few days of life, which could be related, in part, to immaturity of the baroreflex. In the present study, we investigated the baroreflex control of fetal heart rate and renal sympathetic nerve activity (RSNA) in preterm fetal sheep in utero (102 +/- 1 days of gestation; term 140 days). Phenylephrine was associated with a significant increase in BP from 38 +/- 2 to 58 +/- 3 mmHg and a decrease in heart rate (HR) from 177 +/- 4 to 116 +/- 8 beats per minute (bpm). Sodium nitroprusside was associated with a significant fall in BP from 38 +/- 2 to 26 +/- 1 mmHg and an increase in HR from 182 +/- 4 to 274 +/- 8 bpm. However, the time between the 50% changes in BP and HR was significantly greater after hypotension than hypertension (31 +/- 8 s vs. 14 +/- 5 s, P < 0.05). No significant changes in RSNA occurred with either stimulus. This suggests that there are different maturational tempos for the components of the central autonomic response to altered blood pressure.

  17. Systemic and renal-specific sympathoinhibition in obesity hypertension.

    Science.gov (United States)

    Lohmeier, Thomas E; Iliescu, Radu; Liu, Boshen; Henegar, Jeffrey R; Maric-Bilkan, Christine; Irwin, Eric D

    2012-02-01

    Chronic pressure-mediated baroreflex activation suppresses renal sympathetic nerve activity. Recent observations indicate that chronic electric activation of the carotid baroreflex produces sustained reductions in global sympathetic activity and arterial pressure. Thus, we investigated the effects of global and renal specific suppression of sympathetic activity in dogs with sympathetically mediated, obesity-induced hypertension by comparing the cardiovascular, renal, and neurohormonal responses to chronic baroreflex activation and bilateral surgical renal denervation. After control measurements, the diet was supplemented with beef fat, whereas sodium intake was held constant. After 4 weeks on the high-fat diet, when body weight had increased ≈50%, fat intake was reduced to a level that maintained this body weight. This weight increase was associated with an increase in mean arterial pressure from 100±2 to 117±3 mm Hg and heart rate from 86±3 to 130±4 bpm. The hypertension was associated with a marked increase in cumulative sodium balance despite an approximately 35% increase in glomerular filtration rate. The importance of increased tubular reabsorption to sodium retention was further reflected by ≈35% decrease in fractional sodium excretion. Subsequently, both chronic baroreflex activation (7 days) and renal denervation decreased plasma renin activity and abolished the hypertension. However, baroreflex activation also suppressed systemic sympathetic activity and tachycardia and reduced glomerular hyperfiltration while increasing fractional sodium excretion. In contrast, glomerular filtration rate increased further after renal denervation. Thus, by improving autonomic control of cardiac function and diminishing glomerular hyperfiltration, suppression of global sympathetic activity by baroreflex activation may have beneficial effects in obesity beyond simply attenuating hypertension.

  18. [Nerve growth factor and the physiology of pain: the relationships among interoception, sympathetic neurons and the emotional response indicated by the molecular pathophysiology of congenital insensitivity to pain with anhidrosis].

    Science.gov (United States)

    Indo, Yasuhiro

    2015-05-01

    Nerve growth factor (NGF) is a neurotrophic factor essential for the survival and maintenance of neurons. Congenital insensitivity to pain with anhidrosis (CIPA) is caused by loss-of-function mutations in NTRK1, which encodes a receptor tyrosine kinase, TrkA, for NGF. Mutations in NTRK1 cause the selective loss of NGF-dependent neurons, including both NGF-dependent primary afferents and sympathetic postganglionic neurons, in otherwise intact systems. The NGF-dependent primary afferents are thinly myelinated AΔ or unmyelinated C-fibers that are dependent on the NGF-TrkA system during development. NGF-dependent primary afferents are not only nociceptive neurons that transmit pain and temperature sensation, but also are polymodal receptors that play essential roles for interoception by monitoring various changes in the physiological status of all tissues in the body. In addition, they contribute to various inflammatory processes in acute, chronic and allergic inflammation. Together with sympathetic postganglionic neurons, they maintain the homeostasis of the body and emotional responses via interactions with the brain, immune and endocrine systems. Pain is closely related to emotions that accompany physical responses induced by systemic activation of the sympathetic nervous system. In contrast to a negative image of emotions in daily life, Antonio Damasio proposed the 'Somatic Marker Hypothesis', wherein emotions play critical roles in the decision-making and reasoning processes. According to this hypothesis, reciprocal communication between the brain and the body-proper are essential for emotional responses. Using the pathophysiology of CIPA as a foundation, this article suggests that NGF-dependent neurons constitute a part of the neuronal network required for homeostasis and emotional responses, and indicates that this network plays important roles in mediating the reciprocal communication between the brain and the body-proper.

  19. 交感神经型颈椎病及相关疾病的系统康复%Systematic rehabilitation of sympathetic nerve type of cervical spondylopathy and related diseases

    Institute of Scientific and Technical Information of China (English)

    王高岸; 王恒; 周雪莲

    2003-01-01

    @@ INTRODUCTION There are many symptoms of sympathetic nerve type of cervical spondylopathy, most of which are subjective symptoms and one of the most common symptom is flustered, chest distress. Disease condition is often prolonged, main symptoms of disturbance of posterior thoracic vertebrae joints are back pain and chest distress. Diagnosis of both diseases are mainly according to clinical manifestation, but some symptoms aren't typical and often missed or misdiagnosed. Some patients with disturbance of posterior thoracic vertebrae don' t present with obvious back pain but chest distress, If complicated with cervical spondylopathy, all symptoms are explained with cervical spondylopathy and disturbance of posterior thoracic vertebrae joints is neglected that will lead to prolongation.

  20. Renal denervation and hypertension.

    Science.gov (United States)

    Schlaich, Markus P; Krum, Henry; Sobotka, Paul A; Esler, Murray D

    2011-06-01

    Essential hypertension remains one of the biggest challenges in medicine with an enormous impact on both individual and society levels. With the exception of relatively rare monogenetic forms of hypertension, there is now general agreement that the condition is multifactorial in nature and hence requires therapeutic approaches targeting several aspects of the underlying pathophysiology. Accordingly, all major guidelines promote a combination of lifestyle interventions and combination pharmacotherapy to reach target blood pressure (BP) levels in order to reduce overall cardiovascular risk in affected patients. Although this approach works for many, it fails in a considerable number of patients for various reasons including drug-intolerance, noncompliance, physician inertia, and others, leaving them at unacceptably high cardiovascular risk. The quest for additional therapeutic approaches to safely and effectively manage hypertension continues and expands to the reappraisal of older concepts such as renal denervation. Based on the robust preclinical and clinical data surrounding the role of renal sympathetic nerves in various aspects of BP control very recent efforts have led to the development of a novel catheter-based approach using radiofrequency (RF) energy to selectively target and disrupt the renal nerves. The available evidence from the limited number of uncontrolled hypertensive patients in whom renal denervation has been performed are auspicious and indicate that the procedure has a favorable safety profile and is associated with a substantial and presumably sustained BP reduction. Although promising, a myriad of questions are far from being conclusively answered and require our concerted research efforts to explore the full potential and possible risks of this approach. Here we briefly review the science surrounding renal denervation, summarize the current data on safety and efficacy of renal nerve ablation, and discuss some of the open questions that need

  1. Lower limb pain in sympathetic-sensory coupling

    Institute of Scientific and Technical Information of China (English)

    Hongjun Yang; Kairun Peng; Sanjue Hu; Li Xuan

    2011-01-01

    Previous studies have shown that sympathetic nerves are related to certain types of pain, and this phenomenon is referred to as sympathetic-sensory coupling. Chronic pain resulting from nerve injury can be exacerbated by sympathetic stimulation or relieved by sympathetic inhibition. In the present study, the correlation between pain and sympathetic nerves was analyzed in patients with severe pain in lower limbs, as well as in a chronically compressed dorsal root ganglion (CCD) rat model (model of low back pain and sciatica). Patients with severe pain in the lower limbs underwent chemical lumbar sympathectomy (CLS), and the analgesic effects of CLS were compared with painkillers. Results demonstrated significantly relieved lower limb pain following CLS, and the analgesic effects of CLS were superior to those seen with painkillers. In the CCD rat model, dorsal root ganglion neuronal activity significantly increased as a result of electrical stimulation to the sympathetic nerves. These results suggest that sympathetic nerves are closely associated with pain and sympathetic-sensory coupling is likely in lower limb pain in both patients and rat models of CCD.

  2. Protein kinase C pathway on cardiac sympathetic nerve neuroplasticity and myocardial interstitial remodeling%心脏交感神经和心肌间质重塑的共同通路——蛋白激酶C途径

    Institute of Scientific and Technical Information of China (English)

    李贺; 周欣; 王坷; 赵丽霞; 王志宏; 李玉明

    2011-01-01

    Cardiac sympathetic nerve and myocardial interstitium play important roles for preservation of heart function. Different extent of the interstitial remodeling and neuroplasticity commonly occur in many kinds of cardiovascular diseases. The abnormalities interact and contribute to progression and worsening of the diseases. There is accumulating evidence suggesting that protein kinase C activation as a regulator involves in and mediates interaction between the neuroplasticity and remodeling under such conditions, which plays a critical role in the nerve dysfunction and myocardial fibrosis.%心脏交感神经和心肌间质对维持正常心功能有重要作用.心血管患病时,两者均发生不同程度的重塑,并互相影响,这些变化对疾病进展发挥重要影响.研究证据显示,两者间的相互作用可能通过蛋白激酶C介导,对交感神经功能异常和心肌纤维化都发挥重要作用.

  3. Renal denervation attenuates NADPH oxidase-mediated oxidative stress and hypertension in rats with hydronephrosis.

    Science.gov (United States)

    Peleli, Maria; Al-Mashhadi, Ammar; Yang, Ting; Larsson, Erik; Wåhlin, Nils; Jensen, Boye L; G Persson, A Erik; Carlström, Mattias

    2016-01-01

    Hydronephrosis is associated with the development of salt-sensitive hypertension. Studies have suggested that increased sympathetic nerve activity and oxidative stress play important roles in hypertension and the modulation of salt sensitivity. The present study primarily aimed to examine the role of renal sympathetic nerve activity in the development of hypertension in rats with hydronephrosis. In addition, we aimed to investigate if NADPH oxidase (NOX) function could be affected by renal denervation. Partial unilateral ureteral obstruction (PUUO) was created in 3-wk-old rats to induce hydronephrosis. Sham surgery or renal denervation was performed at the same time. Blood pressure was measured during normal, high-, and low-salt diets. The renal excretion pattern, NOX activity, and expression as well as components of the renin-angiotensin-aldosterone system were characterized after treatment with the normal salt diet. On the normal salt diet, rats in the PUUO group had elevated blood pressure compared with control rats (115 ± 3 vs. 87 ± 1 mmHg, P Renal denervation in PUUO rats attenuated both hypertension (97 ± 3 mmHg) and salt sensitivity (5 ± 1 mmHg, P renal excretion pattern, whereas the degree of renal fibrosis and inflammation was not changed. NOX activity and expression as well as renin and ANG II type 1A receptor expression were increased in the renal cortex from PUUO rats and normalized by denervation. Plasma Na(+) and K(+) levels were elevated in PUUO rats and normalized after renal denervation. Finally, denervation in PUUO rats was also associated with reduced NOX expression, superoxide production, and fibrosis in the heart. In conclusion, renal denervation attenuates hypertension and restores the renal excretion pattern, which is associated with reduced renal NOX and components of the renin-angiotensin-aldosterone system. This study emphasizes a link between renal nerves, the development of hypertension, and modulation of NOX function.

  4. Endoplasmic reticulum stress increases brain MAPK signaling, inflammation and renin-angiotensin system activity and sympathetic nerve activity in heart failure.

    Science.gov (United States)

    Wei, Shun-Guang; Yu, Yang; Weiss, Robert M; Felder, Robert B

    2016-10-01

    We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of heart failure (HF) rats and is reduced by inhibition of mitogen-activated protein kinase (MAPK) signaling. The present study further examined the relationship between brain MAPK signaling, ER stress, and sympathetic excitation in HF. Sham-operated (Sham) and HF rats received a 4-wk intracerebroventricular (ICV) infusion of vehicle (Veh) or the ER stress inhibitor tauroursodeoxycholic acid (TUDCA, 10 μg/day). Lower mRNA levels of the ER stress biomarkers GRP78, ATF6, ATF4, and XBP-1s in the SFO and PVN of TUDCA-treated HF rats validated the efficacy of the TUDCA dose. The elevated levels of phosphorylated p44/42 and p38 MAPK in SFO and PVN of Veh-treated HF rats, compared with Sham rats, were significantly reduced in TUDCA-treated HF rats as shown by Western blot and immunofluorescent staining. Plasma norepinephrine levels were higher in Veh-treated HF rats, compared with Veh-treated Sham rats, and were significantly lower in the TUDCA-treated HF rats. TUDCA-treated HF rats also had lower mRNA levels for angiotensin converting enzyme, angiotensin II type 1 receptor, tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, and NF-κB p65, and a higher mRNA level of IκB-α, in the SFO and PVN than Veh-treated HF rats. These data suggest that ER stress contributes to the augmented sympathetic activity in HF by inducing MAPK signaling, thereby promoting inflammation and renin-angiotensin system activity in key cardiovascular regulatory regions of the brain.

  5. Severe hemorrhage attenuates cardiopulmonary chemoreflex control of regional sympathetic outputs via NTS adenosine receptors.

    Science.gov (United States)

    Minic, Zeljka; Li, Cailian; O'Leary, Donal S; Scislo, Tadeusz J

    2014-09-15

    Selective stimulation of inhibitory A1 and facilitatory A2a adenosine receptor subtypes located in the nucleus of the solitary tract (NTS) powerfully inhibits cardiopulmonary chemoreflex (CCR) control of regional sympathetic outputs via different mechanisms: direct inhibition of glutamate release and facilitation of an inhibitory neurotransmitter release, respectively. However, it remains unknown whether adenosine naturally released into the NTS has similar inhibitory effects on the CCR as the exogenous agonists do. Our previous study showed that adenosine is released into the NTS during severe hemorrhage and contributes to reciprocal changes of renal (decreases) and adrenal (increases) sympathetic nerve activity observed in this setting. Both A1 and A2a adenosine receptors are involved. Therefore, we tested the hypothesis that, during severe hemorrhage, CCR control of the two sympathetic outputs is attenuated by adenosine naturally released into the NTS. We compared renal and adrenal sympathoinhibitory responses evoked by right atrial injections of 5HT3 receptor agonist phenylbiguanide (2-8 μg/kg) under control conditions, during hemorrhage, and during hemorrhage preceded by blockade of NTS adenosine receptors with bilateral microinjections of 8-(p-sulfophenyl) theophylline (1 nmol/100 nl) in urethane/chloralose anesthetized rats. CCR-mediated inhibition of renal and adrenal sympathetic activity was significantly attenuated during severe hemorrhage despite reciprocal changes in the baseline activity levels, and this attenuation was removed by bilateral blockade of adenosine receptors in the caudal NTS. This confirmed that adenosine endogenously released into the NTS has a similar modulatory effect on integration of cardiovascular reflexes as stimulation of NTS adenosine receptors with exogenous agonists.

  6. Effect of catheter-based renal sympathetic denervation in pigs with rapid pacing induced heart failure%肾交感神经射频消融术治疗快速起搏致猪心力衰竭的疗效

    Institute of Scientific and Technical Information of China (English)

    谢赟; 刘奇良; 徐佑龙; 郜俊清; 严鹏勇; 张文全; 孙剑光; 王明瑜; 金惠根

    2014-01-01

    at 1 and 2 weeks post pacing.Serum biochemical markers including renin,aldosterone and creatinine were also measured at baseline,1 and 2 weeks after pacing.Repeated renal artery angiography was performed at 1 week after RDN.All pigs were sacrificed to examine the heart and renal pathology and renal artery sympathetic nerve staining at 2 weeks post pacing.Results LVEF decreased 1 week after rapid pacing from (60.5 ± 6.0) % to (35.3 ± 9.8) %.LVEF was significantly higher [(42.8 ± 5.9) % vs.(33.4 ± 9.7) %,P =0.001 8] while LVESD was significantly lower [(28.4 ±3.7) mm vs.(33.0 ±2.0) mm,P =0.001 6] in the RDN group than in the control group at 2 weeks post pacing.At 2 weeks after pacing,plasma concentrations of renin and aldersterone were significantly lower in RDN group compared to the control group (all P < 0.05).Kidney function and blood pressure were comparable between the two groups at 2 weeks post pacing.There were no signs of renal damages such as renal artery stenosis,dissection and thrombus in all pigs after 2 weeks pacing.Sympathetic neurons of adventitia were injured in RND group.Conclusion RDN could significantly improve cardiac function and attenuate left ventricular remodeling via inhibiting renin-angiotensin-aldosterone system in this pacing induced pig heart failure model.

  7. TRPA1 Mediates Amplified Sympathetic Responsiveness to Activation of Metabolically Sensitive Muscle Afferents in Rats with Femoral Artery Occlusion

    Directory of Open Access Journals (Sweden)

    Jihong eXing

    2015-09-01

    Full Text Available Autonomic responses to stimulation of mechanically and metabolically sensitive muscle afferent nerves during static contraction are augmented in rats with femoral artery occlusion. Moreover, metabolically sensitive transient receptor potential cation channel subfamily A, member 1 (TRPA1 has been reported to contribute to sympathetic nerve activity (SNA and arterial blood pressure (BP responses evoked by static muscle contraction. Thus, in the present study, we examined the mechanisms by which afferent nerves’ TRPA1plays a role in regulating amplified sympathetic responsiveness due to a restriction of blood flow directed to the hindlimb muscles. Our data show that 24-72 hrs of femoral artery occlusion 1 upregulates the protein levels of TRPA1 in dorsal root ganglion (DRG tissues; 2 selectively increases expression of TRPA1 in DRG neurons supplying metabolically sensitive afferent nerves of C-fiber (group IV; and 3 enhances renal SNA and BP responses to AITC (a TRPA1 agonist injected into the arterial blood supply of the hindlimb muscles. In addition, our data demonstrate that blocking TRPA1 attenuates SNA and BP responses during muscle contraction to a greater degree in ligated rats than those responses in control rats. In contrast, blocking TRPA1 fails to attenuate SNA and BP responses during passive tendon stretch in both groups. Overall, results of this study indicate that alternations in muscle afferent nerves’TRPA1 likely contribute to enhanced sympathetically mediated autonomic responses via the metabolic component of the muscle reflex under circumstances of chronic muscle ischemia.

  8. 中医治疗反射性交感神经营养不良56例临床观察%Clinical Observation on Traditional Chinese Medicine in Treatment of 56 Cases With Reflexive Sympathetic Nerve Malnutrition

    Institute of Scientific and Technical Information of China (English)

    樊璠

    2015-01-01

    目的 观察中医治疗反射性交感神经营养不良的临床效果.方法 选择2014年8月~2015年3月我院收治的反射性交感神经营养不良患者56例作为研究对象.将患者随机分为对照组和观察组,各28例.对照组应用常规西医治疗,观察组应用中医综合治疗.两组患者均接受为期1个月的治疗,对比治疗周期结束后两组患者在临床疗效方面的差异.结果 观察组临床治疗总有效率为96.43%(27/28),对照组为71.43%(20/28).观察组临床治疗效果优于对照组,P<0.05,差异具有统计学意义.结论 应用中药内服联合熏洗治疗反射性交感神经营养不良的临床效果确切,可在短期内达到满意疗效.%Objective Clinical Observation on the traditional Chinese medicine in treatment of reflexive sympathetic nerve malnutrition. Methods Selected 56 patients with reflexive sympathetic nerve malnutrition from August 2014 to March 2015 in our hospital, randomly were divided into the control group and the observation group, each group had 28 cases. the control group used conventional western medicine treatment, the observation group used comprehensive traditional Chinese medicine. Two groups of patients were treated for 1 month. Compared cycle differences in clinical efficacy of two groups after treatment.Results The observation group of patients clinical total effective rate was 96.43% (20/28), the control group was 71.43% (27/28), the observation group clinical treatment effect was better than the control group,P<0.05, was difference had statistically significance. Conclusion The application of combined fumigation treatment of traditional Chinese medicine internal and the clinical effect of exact reflection sexual intercourse feeling nervous malnutrition, can achieve satisfactory curative effect in the short term.

  9. Catheter-based renal sympathetic denervation for resistant hypertension in chronic renal failure:recent progress in clinical research%肾交感射频消融术在慢性肾脏病患者高血压治疗的应用研究

    Institute of Scientific and Technical Information of China (English)

    柏雨双; 甘华

    2014-01-01

    交感神经过度兴奋与慢性肾脏疾病(chronic kidney disease,CKD)患者高血压的发生、发展密切相关.而抗交感药物难以达到降压治疗目标.近年来,肾交感射频消融术(catheter-based renal sympathetic denervation,RSD)迅猛发展,成为了CKD患者治疗高血压新的尝试.本文对此项技术在CKD患者高血压治疗的应用进行探讨.

  10. Intermedin in paraventricular nucleus attenuates sympathetic activity and blood pressure via nitric oxide in hypertensive rats.

    Science.gov (United States)

    Zhou, Ye-Bo; Sun, Hai-Jian; Chen, Dan; Liu, Tong-Yan; Han, Ying; Wang, Jue-Jin; Tang, Chao-Shu; Kang, Yu-Ming; Zhu, Guo-Qing

    2014-02-01

    Intermedin (IMD) is a member of calcitonin/calcitonin gene-related peptide family, which shares the receptor system consisting of calcitonin receptor-like receptor (CRLR) and receptor activity-modifying proteins (RAMPs). This study investigated the effects of IMD in paraventricular nucleus (PVN) on renal sympathetic nerve activity and mean arterial pressure and its downstream mechanism in hypertension. Rats were subjected to 2-kidney 1-clip (2K1C) surgery to induce renovascular hypertension or sham operation. Acute experiments were performed 4 weeks later under anesthesia. IMD mRNA and protein were downregulated in 2K1C rats. Bilateral PVN microinjection of IMD caused greater decreases in renal sympathetic nerve activity and mean arterial pressure in 2K1C rats than in sham-operated rats, which were prevented by pretreatment with adrenomedullin receptor antagonist AM22-52 or nonselective nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester, and attenuated by selective neuronal NO synthase inhibitor N(ω)-propyl-l-arginine hydrochloride or endothelial NO synthase inhibitor N(5)-(1-iminoethyl)-l-ornithine dihydrochloride. AM22-52 increased renal sympathetic nerve activity and mean arterial pressure in 2K1C rats but not in sham-operated rats, whereas calcitonin/calcitonin gene-related peptide receptor antagonist calcitonin/calcitonin gene-related peptide 8-37 had no significant effect. CRLR and RAMP3 mRNA, as well as CRLR, RAMP2, and RAMP3 protein expressions, in the PVN were increased in 2K1C rats. Microinjection of IMD into the PVN increased the NO metabolites (NOx) level in the PVN in 2K1C rats, which was prevented by AM22-52. Chronic PVN infusion of IMD reduced, but AM22-52 increased, blood pressure in conscious 2K1C rats. These results indicate that IMD in the PVN inhibits sympathetic activity and attenuates hypertension in 2K1C rats, which are mediated by adrenomedullin receptors (CRLR/RAMP2 or CRLR/RAMP3) and its downstream NO.

  11. [Nucleotide receptors and renal function].

    Science.gov (United States)

    Jankowski, Maciej

    2014-01-01

    Kidney plays a key role in homeostasis of human body. It has heterogenic structure and is characterized by complicated vascular beds and numbers of sympathetic nerves endings. Nucleotides receptors are involved in the regulation of blood flow, a fundamental process for renal function. Plasma is filtrated in renal glomerulus and activity of nucleotides receptors located on cells of glomerular filter modifies the physi- cochemical properties of filter and affects the filtration process. Electrolytes, water and low molecular weight molecules are reabsorbed from tubular fluid or secreted into fluid in proximal and distal tubules. Glomerular filtration rate and activity of tubular processes are regulated via nucleotides receptors by glomerulotubularbalance and tubuloglomerular feedback. Nucleotides receptors are involved in systemic regulation of blood pressure and carbohydrate metabolism.

  12. Renal denervation in the treatment of resistant hypertension: Dead, alive or surviving?

    Science.gov (United States)

    Al-Fakhouri, Ahmad; Efeovbokhan, Nephertiti; Nakhla, Rami; Khouzam, Rami N

    2016-10-01

    Hypertension is one of the most common chronic clinical problems encountered by physicians. The prevalence of resistant hypertension is estimated at 9% in the US. Patients with resistant hypertension have been shown to be at higher risk for adverse cardiovascular events, hence the need for greater efforts in improving the treatment of hypertension. The renal sympathetic nerves play an important role in the development of hypertension, mediated via sodium and water retention, increased renin release and alterations in renal blood flow. The proximity of the afferent and efferent renal sympathetic nerves to the adventitia of the renal arteries suggested the feasibility of an endovascular, selective, minimally invasive approach to renal denervation; a potential treatment option for resistant hypertension. While the RAPID, Reduce-HTN, EnligHTN, DENERHTN and Symplicity HTN-1 and -2 studies showed significant benefit of renal denervation in the treatment of resistant hypertension, the results of Oslo RDN, Prague-15 and Symplicity HTN-3 were not so favorable. Future well-designed clinical trials are needed to ascertain the benefits or otherwise of renal denervation in treatment-resistant hypertension.

  13. The Human Sympathetic Nervous System Response to Spaceflight

    Science.gov (United States)

    Ertl, Andrew C.; Diedrich, Andre; Paranjape, Sachin Y.; Biaggioni, Italo; Robertson, Rose Marie; Lane, Lynda D.; Shiavi, Richard; Robertson, David

    2003-01-01

    The sympathetic nervous system is an important part of the autonomic (or automatic) nervous system. When an individual stands up, the sympathetic nervous system speeds the heart and constricts blood vessels to prevent a drop in blood pressure. A significant number of astronauts experience a drop in blood pressure when standing for prolonged periods after they return from spaceflight. Difficulty maintaining blood pressure with standing is also a daily problem for many patients. Indirect evidence available before the Neurolab mission suggested the problem in astronauts while in space might be due partially to reduced sympathetic nervous system activity. The purpose of this experiment was to identify whether sympathetic activity was reduced during spaceflight. Sympathetic nervous system activity can be determined in part by measuring heart rate, nerve activity going to blood vessels, and the release of the hormone norepinephrine into the blood. Norepinephrine is a neurotransmitter discharged from active sympathetic nerve terminals, so its rate of release can serve as a marker of sympathetic nervous system action. In addition to standard cardiovascular measurements (heart rate, blood pressure), we determined sympathetic nerve activity as well as norepinephrine release and clearance on four crewmembers on the Neurolab mission. Contrary to our expectation, the results demonstrated that the astronauts had mildly elevated resting sympathetic nervous system activity in space. Sympathetic nervous system responses to stresses that simulated the cardiovascular effects of standing (lower body negative pressure) were brisk both during and after spaceflight. We concluded that, in the astronauts tested, the activity and response of the sympathetic nervous system to cardiovascular stresses appeared intact and mildly elevated both during and after spaceflight. These changes returned to normal within a few days.

  14. [The somato-sympathetic and somato-somatic reflexes in the spontaneous hypertensive rats].

    Science.gov (United States)

    Shcherbin, Iu I; Tsyrlin, V A

    2014-01-01

    In anaesthetized normotensive (Wistar) and hypertensive (SHR) rats, sympathetic and somatic reflexes were studied before and after cervical spinal cord transection. Single shock stimulation of a peripheral afferent nerve of brachial plexus produced reflex discharges in the cervical sympathetic trunk and the radial nerve. In rats with intact brain stem, evoked response in the cervical sympathetic trunk was composed of three components, but evoked response in radial nerve consisted of two components. The total somato-sympathetic reflex in hypertensive rats was more on 54 % than the somato-sympathetic reflex in normotensive rats. The total somato-somatic reflex in hypertensive rats was more on 70 % than the somato-somatic reflex in normotensive rats. In rats with transected brain stem, evoked response in the cervical sympathetic trunk was composed of two components, but evoked response in radial nerve consisted of one component. After neuraxis transection the total sympathetic and somatic reflexes in normotensive rats decreased by 85 and 83 %, respectively. The total sympathetic and somatic reflexes in hypertensive rats decreased by 88 and 84 %, respectively. However, the peak value of evoked discharges in sympathetic and somatic nerves were more in hypertensive rats than in normotensive rats. Suprasegmental and spinal mechanisms responsible for the augmentation of both sympathetic and somatic reflexes are discussed.

  15. Sympathetic adaptations to one-legged training

    Science.gov (United States)

    Ray, C. A.

    1999-01-01

    The purpose of the present study was to determine the effect of leg exercise training on sympathetic nerve responses at rest and during dynamic exercise. Six men were trained by using high-intensity interval and prolonged continuous one-legged cycling 4 day/wk, 40 min/day, for 6 wk. Heart rate, mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA; peroneal nerve) were measured during 3 min of upright dynamic one-legged knee extensions at 40 W before and after training. After training, peak oxygen uptake in the trained leg increased 19 +/- 2% (P leg exercise and indicates that attenuation of MSNA to exercise reported with forearm training also occurs with leg training.

  16. Aldosterone-induced brain MAPK signaling and sympathetic excitation are angiotensin II type-1 receptor dependent.

    Science.gov (United States)

    Zhang, Zhi-Hua; Yu, Yang; Wei, Shun-Guang; Felder, Robert B

    2012-02-01

    Angiotensin II (ANG II)-induced mitogen-activated protein kinase (MAPK) signaling upregulates angiotensin II type-1 receptors (AT(1)R) in hypothalamic paraventricular nucleus (PVN) and contributes to AT(1)R-mediated sympathetic excitation in heart failure. Aldosterone has similar effects to increase AT(1)R expression in the PVN and sympathetic drive. The present study was undertaken to determine whether aldosterone also activates the sympathetic nervous system via MAPK signaling and, if so, whether its effect is independent of ANG II and AT(1)R. In anesthetized rats, a 4-h intravenous infusion of aldosterone induced increases (P < 0.05) in phosphorylated (p-) p44/42 MAPK in PVN, PVN neuronal excitation, renal sympathetic nerve activity (RSNA), mean blood pressure (MBP), and heart rate (HR). Intracerebroventricular or bilateral PVN microinjection of the p44/42 MAPK inhibitor PD-98059 reduced the aldosterone-induced RSNA, HR, and MBP responses. Intracerebroventricular pretreatment (5 days earlier) with pooled small interfering RNAs targeting p44/42 MAPK reduced total and p-p44/42 MAPK, aldosterone-induced c-Fos expression in the PVN, and the aldosterone-induced increases in RSNA, HR, and MBP. Intracerebroventricular infusion of either the mineralocorticoid receptor antagonist RU-28318 or the AT(1)R antagonist losartan blocked aldosterone-induced phosphorylation of p44/42 MAPK and prevented the increases in RSNA, HR, and MBP. These data suggest that aldosterone-induced sympathetic excitation depends upon that AT(1)R-induced MAPK signaling in the brain. The short time course of this interaction suggests a nongenomic mechanism, perhaps via an aldosterone-induced transactivation of the AT(1)R as described in peripheral tissues.

  17. Upregulation of orexin receptor in paraventricular nucleus promotes sympathetic outflow in obese Zucker rats.

    Science.gov (United States)

    Zhou, Jing-Jing; Yuan, Fang; Zhang, Yi; Li, De-Pei

    2015-12-01

    Sympathetic vasomotor tone is elevated in obesity-related hypertension. Orexin importantly regulates energy metabolism and autonomic function. We hypothesized that alteration of orexin receptor in the paraventricular nucleus (PVN) of the hypothalamus leads to elevated sympathetic vasomotor tone in obesity. We used in vivo measurement of sympathetic vasomotor tone and microinjection into brain nucleus, whole-cell patch clamp recording in brain slices, and immunocytochemical staining in obese Zucker rats (OZRs) and lean Zucker rats (LZRs). Microinjection of orexin 1 receptor (OX1R) antagonist SB334867 into the PVN reduced basal arterial blood pressure (ABP) and renal sympathetic nerve activity (RSNA) in anesthetized OZRs but not in LZRs. Microinjection of orexin A into the PVN produced greater increases in ABP and RSNA in OZRs than in LZRs. Western blot analysis revealed that OX1R expression levels in the PVN were significantly increased in OZRs compared with LZRs. OX1R immunoreactivity was positive in retrogradely labeled PVN-spinal neurons. The basal firing rate of labeled PVN-spinal neurons was higher in OZRs than in LZRs. SB334867 decreased the basal firing activity of PVN-spinal neurons in OZRs but had no effect in LZRs. Orexin A induced a greater increase in the firing rate of PVN-spinal neurons in OZRs than in LZRs. In addition, orexin A induced larger currents in PVN-spinal neurons in OZRs than in LZRs. These data suggest that upregulation of OX1R in the PVN promotes hyperactivity of PVN presympathetic neurons and elevated sympathetic outflow in obesity.

  18. The effects of chronic intermittent hypoxia on blood pressure and sympathetic nerve activity in rats%慢性间歇低氧对大鼠血压和交感神经兴奋性的影响

    Institute of Scientific and Technical Information of China (English)

    万南生; 陈宝元; 冯靖; 李硕; 周伟; 张祯; 郭润

    2012-01-01

    目的 通过观察不同程度慢性间歇低氧(chronic intermittent hypoxia,CIH)作用下大鼠血压与交感神经活性水平动态变化,探讨CIH对血压及交感神经活性的影响及血压与交感神经活性之间的相关性,并明确CIH诱发高血压发病的机制.方法 168只雄性6周龄Wistar大鼠,体重160 ~ 180 g,采用随机数字表法分为非暴露组(UD)、重度间歇低氧组(IH1)、中度间歇低氧组(IH2)、轻度间歇低氧组(IH3)、持续低氧组(CH)及对照组,分别给予不同程度和频率的低氧环境.UD组8只大鼠于实验前处死,其余各实验组每组32只大鼠,分别于2、4、6、8周时随机抽取8只处死,留取静脉血抗凝离心后- 80℃保存血浆,并于实验前、实验结束后分别测定动脉收缩压,实验结束后测定血浆中去甲肾上腺素(norepinephrine,NE).结果 各组大鼠实验前收缩压差异无统计学意义(F=0.008,P>0.05),随着实验时间延长,各间歇低氧组大鼠收缩压逐渐升高,4周开始明显高于UD组、对照组及CH组(均P<0.05)且血压水平与低氧程度正相关(F =9.844,P<0.01),IH1组明显高于IH3组(P<0.05),而对照组和CH组无明显改变.各间歇低氧组大鼠血浆NE随实验时间延长而逐渐升高,8周时明显高于UD组、SC组及CH组(均P<0.05或P<0.01),且NE水平与低氧程度正相关(F=11.537,P<0.01),IH1组明显高于IH3组(P<0.05),SC组和CH组大鼠血浆NE变化不显著.大鼠血浆NE与血压呈显著正相关(r=0.538,P<0.01).结论 CIH作用可以引起大鼠血压增高和交感活性增强且存在明显的低氧程度依赖性和时间过程规律性,推测CIH引起大鼠血压增高可能与交感活性增强相关.%Objective To observe the changes of blood pressure and sympathetic nerve activity under different degrees of chronic intermittent hypoxia (CIH) in rats,and therefore to explore the effects of CIH on blood pressure and sympathetic nerve activity and the correlation between

  19. NTS adenosine A2a receptors inhibit the cardiopulmonary chemoreflex control of regional sympathetic outputs via a GABAergic mechanism.

    Science.gov (United States)

    Minic, Zeljka; O'Leary, Donal S; Scislo, Tadeusz J

    2015-07-01

    Adenosine is a powerful central neuromodulator acting via opposing A1 (inhibitor) and A2a (activator) receptors. However, in the nucleus of the solitary tract (NTS), both adenosine receptor subtypes attenuate cardiopulmonary chemoreflex (CCR) sympathoinhibition of renal, adrenal, and lumbar sympathetic nerve activity and attenuate reflex decreases in arterial pressure and heart rate. Adenosine A1 receptors inhibit glutamatergic transmission in the CCR pathway, whereas adenosine A2a receptors most likely facilitate release of an unknown inhibitory neurotransmitter, which, in turn, inhibits the CCR. We hypothesized that adenosine A2a receptors inhibit the CCR via facilitation of GABA release in the NTS. In urethane-chloralose-anesthetized rats (n = 51), we compared regional sympathetic responses evoked by stimulation of the CCR with right atrial injections of the 5-HT3 receptor agonist phenylbiguanide (1-8 μg/kg) before and after selective stimulation of NTS adenosine A2a receptors [microinjections into the NTS of CGS-21680 (20 pmol/50 nl)] preceded by blockade of GABAA or GABAB receptors in the NTS [bicuculline (10 pmol/100 nl) or SCH-50911 (1 nmol/100 nl)]. Blockade of GABAA receptors virtually abolished adenosine A2a receptor-mediated inhibition of the CCR. GABAB receptors had much weaker but significant effects. These effects were similar for the different sympathetic outputs. We conclude that stimulation of NTS adenosine A2a receptors inhibits CCR-evoked hemodynamic and regional sympathetic reflex responses via a GABA-ergic mechanism.

  20. 刃针配合刮痧治疗交感神经型颈椎病100例%100 Cases of Sympathetic Nerve Type of Cervical Spondylosis Treated with Blade Needle Therapy and Guasha Therapy

    Institute of Scientific and Technical Information of China (English)

    叶花苓

    2015-01-01

    Objective To observe the clinical efficacy on sympathetic nerve type of cervical spondy-losis(SNCS)treated with blade needle therapy and guasha therapy. Methods Two hundred patients of SNCS were randomized into a treatment group(100 cases)and a control group(100 cases). In the treatment group, the blade needle therapy,massage and guasha therapy were used in combination. In the control group,the blade needle therapy and massage were applied. Results The total effective rate was 98% in the treatment group and was 86% . The efficacy in the treatment group was obviously better than that in the control group, indicating the significant difference(P ﹤ 0. 05). Conclusion The blade needle therapy combined with mas-sage and guasha therapy achieves the apparent better efficacy on SNCS in comparison with the simple blade needle therapy and massage.%目的:观察刃针配合刮痧治疗交感神经型颈椎病的临床疗效。方法选取患交感神经型颈椎病的患者200例随机分为治疗组100例和对照组100例,治疗组采用刃针推拿配合刮痧治疗,对照组采用单纯刃针推拿治疗。结果治疗组总有效率98%,对照组总有效率86%,治疗组疗效明显优于对照组,两组比较,差异有统计学意义(P ﹤0.05)。结论刃针推拿配合刮痧治疗交感神经型颈椎病疗效明显优于单纯刃针推拿治疗。

  1. 去肾上腺素能交感神经支配对大鼠良性增生前列腺的影响%Damage induced by losing innervation of sympathetic nerve in rats' benign hyperplastic prostate

    Institute of Scientific and Technical Information of China (English)

    蔡建良; 辛殿祺; 何群; 汤秀琴; 那彦群

    2008-01-01

    目的 探索去除肾上腺素能交感神经支配后大鼠良性增生前列腺的组织、细胞病理学变化.方法 30周龄雄性自发性高血压大鼠65只,随机分配为手术组、手术对照组和正常对照组.手术组切断双侧盆腔主要神经节的交感腹下神经来源支,然后行膀胱造口术;手术对照组仅行膀胱造口术.分别于术后3、7、11、15、≥21 d分批处死大鼠,观察各组大鼠前列腺大体形态学、组织学和细胞超微结构改变.结果 大鼠实验模型均制作成功.手术组大鼠前列腺在后期(手术15 d后)出现轻微的质地变硬,颜色和形状变化不明显,前列腺湿重/大鼠体重比值随术后时间的延长有下降趋势,前列腺组织干重/湿重比值在手术15 d后逐渐升高,但与手术对照组比较差异均无统计学意义.镜下观:手术组大鼠前列腺早期出现腺腔明显扩张、前列腺液积存和凝块形成,平滑肌拉长变薄,但后期病变逐步缓解,腺上皮层无变化.透射电镜:手术组大鼠前列腺腺细胞、基底膜无明显变化,但平滑肌术后3 d出现肌膜皱缩,肌丝、密体和密斑结构不清晰等改变,术后11 d后,病变逐步好转.手术对照组无上述变化.结论 彻底去除肾上腺素能交感神经支配后,大鼠良性增生前列腺的平滑肌出现短时间的结构受损和功能障碍,后期能自行部分恢复.%Objective To study the pathologic change of rats' benign hyperplastic prostate after losing the innervation of sympathetic nerve. Methods A total of 65 male spontaneous hypertension rats (SHR) aged 30 weeks old were randomly assigned into treatment group, sham surgery control group and normal control group. In treatment group, the originating branches of sympathetic hypngastric nerve of the bilateral major pelvic ganglions were truncated following the performance of eystostomy. The rata were sac-rificed at day 3,7,11,15 and≥21 post-operation respectively. The gross

  2. 卡维地洛对心肌梗死后窦性心率震荡的影响%Effects and relations of carvedilol on heart rate turbulence and secretion of sympathetic nerve in patients with myocardial infarction

    Institute of Scientific and Technical Information of China (English)

    周惠云; 甄胜西; 舒平; 胡金森; 贾少微; 费贤翠; 余小平

    2008-01-01

    Objective To investigate the effects and relations of carvedilol on heart rate turbulence and secretion of sympathetic nerve in patients with myocardial infarction. Methods Sixty-six patients selected with acute myocardial infarction were randomized to enroll into experimental group ( n = 33 ) treated with earvedilol and control group( n = 33 ) treated with metoprolol for 12 months follow-up treatment. The concenrrarions of plasma norepinephrine(NE) and epinephrine (E) and 24 hour Holter monitoring were messured respectively before the treatment ,after 6 months and 12 months; and new cardiac events were supervised for all cases. Quantification of heart rate turbulenee(HRT) were carried out by computer analyzing two factors: turbulence onset(TO) and turbulence slope(TS) from the data of 24 hour Holter monitoring. NE,E,TO,TS and the occurrence rate of new cardiac events were compared between two groups and in different times of treatment. The correlation between TO,TS and NE,E was analysed. Results Before the treatment, there was no significant differences between two groups to the comparisons of NE,E,TO and TS(P>0.05). After treating 6 and 12 months, NE, E and TO of experimental group were all lower than control group's significantly, accordingly TS were all higher(P<0.05). By comparing 3 times( before,after 6 and 12 months of treatment), NE, E and TO of two groups dropped, meanwhile TS rose; experimental group showed significant changes( P<0.05 ), but control group showed no significant differences(P>0.05 ). The occurrence rate of new cardiac events of experimental group was lower than control group's significantly (P<0.05 ).There was significant correlation between NE, E and TO, TS (P<0.05 ). Conclusion Carvedilol treatment can block the secretion of sympathetic nerve after myocardial infarction and prevent the occurrences of new cardiac events significantly; the changes of the secretion of sympathetic nerve can play an important role for heart rate

  3. Splanchnic and renal elimination and release of catecholamines in cirrhosis. Evidence of enhanced sympathetic nervous activity in patients with decompensated cirrhosis

    DEFF Research Database (Denmark)

    Ring-Larsen, H; Kanstrup, I L; Christensen, N J

    1984-01-01

    Plasma noradrenaline (NA) and adrenaline (A) concentrations were determined in different vascular areas in 32 patients with cirrhosis and in nine controls during a right sided heart, liver, and renal vein catheterisation. The patients were divided into four groups: (I) Compensated (without ascites......, respectively, the three last mentioned values being significantly raised (p less than 0.01). Median arterial adrenaline concentrations were not significantly increased. In patients arterial-hepatic venous extraction ratios of noradrenaline and adrenaline were on the average 25% (p less than 0.01) and 20% (p...... differences were significantly increased in groups II, III and IV (0.47, 0.53 and 0.68 nmol/l, p less than 0.01), indicating a significant net release of noradrenaline from the kidneys in recompensated and decompensated patients. Renal extraction of adrenaline was normal. In conclusion, increased arterial...

  4. Microinjection of glycine into the hypothalamic paraventricular nucleus produces diuresis, natriuresis, and inhibition of central sympathetic outflow.

    Science.gov (United States)

    Krowicki, Zbigniew K; Kapusta, Daniel R

    2011-04-01

    Strychnine-sensitive glycine receptors and glycine-immunoreactive fibers are expressed in the hypothalamic paraventricular nucleus (PVN), yet the functional significance of this innervation is unclear. Therefore, these studies examined the changes in cardiovascular and renal function and renal sympathetic nerve activity (RSNA) produced by the microinjection of glycine (5 and 50 nmol) into the PVN of conscious Sprague-Dawley rats. Microinjection of glycine into, but not outside of, the PVN dose-dependently increased urine flow rate and urinary sodium excretion and decreased RSNA. At the higher dose, PVN glycine also decreased heart rate; neither 5 nor 50 nmol PVN glycine altered mean arterial pressure. The glycine (50 nmol)-evoked diuresis and natriuresis were abolished in rats continuously infused intravenously with [Arg(8)]-vasopressin. Furthermore, chronic bilateral renal denervation prevented the bradycardia and diuresis to PVN glycine and blunted the natriuresis. In other studies, unilateral PVN pretreatment with the glycine receptor antagonist strychnine (1.6 nmol) prevented the effects of PVN glycine (50 nmol) on heart rate, RSNA, and renal excretory function. When microinjected bilaterally, PVN strychnine (1.6 nmol per site) evoked a significant increase in heart rate and RSNA without altering renal excretory function. These findings demonstrate that in conscious rats glycine acts in the PVN to enhance the renal excretion of water and sodium and decrease central sympathetic outflow to the heart and kidneys. Although endogenous PVN glycine inputs elicit a tonic control of heart rate and RSNA, the renal excretory responses to PVN glycine seem to be caused primarily by the inhibition of arginine vasopressin secretion.

  5. Blood pressure decrease in spontaneously hypertensive rats folowing renal denervation or dopamine β-hydroxylase inhibition with etamicastat.

    Science.gov (United States)

    Pires, Nuno Miguel; Igreja, Bruno; Moura, Eduardo; Wright, Lyndon Christopher; Serrão, Maria Paula; Soares-da-Silva, Patrício

    2015-09-01

    Overactivity of the sympathetic nervous system has an important role in the development and progression of arterial hypertension. Catheter-based renal nerve ablation for the treatment of drug-resistant hypertension has recently been developed. An alternative strategy for the modulation of sympathetic nerve function is to reduce the biosynthesis of noradrenaline (NA) by inhibiting dopamine β-hydroxylase (DβH), the enzyme that catalyzes the conversion of dopamine (DA) to NA in the sympathetic nerves. Renal denervation (RDN) surgery was performed in spontaneously hypertensive rats (SHR) to evaluate the effect of RDN on the DA and NA levels and on blood pressure over a 28-day period. The selective peripheral DβH inhibitor etamicastat (30 mg kg (-1)day(-1)) was administered to another cohort of SHR. RDN and etamicastat treatment had no effect on the renal function, as assessed by measuring the water balance response, renal function and urinary electrolyte levels. RDN significantly decreased the systolic blood pressure (SBP) and the diastolic blood pressure (DBP). A gradual return of the SBP and the DBP to the high baseline levels was observed over time. Conversely, treatment with etamicastat resulted in a significant decrease in the SBP and the DBP at all time points. On the last day of the assessment, NA levels in renal tissue were significantly decreased in both RDN and etamicastat-treated groups. In contrast, the NA levels in the left ventricle were decreased only in the etamicastat-treated group. Thus, RDN produces transitory decreases in blood pressure, whereas prolonged downregulation of sympathetic drive with the DβH inhibitor etamicastat results in a sustained decrease in the SBP and the DBP.

  6. Carotid baroreceptor-muscle sympathetic relation in humans.

    Science.gov (United States)

    Rea, R F; Eckberg, D L

    1987-12-01

    The purpose of this study was to define the relation between carotid distending pressure and muscle sympathetic activity in humans. Carotid baroreceptors of nine healthy subjects were compressed or stretched for 5 s with graded neck pressure or suction (+40 to -65 mmHg), and muscle sympathetic nerve activity was recorded. The results delineate several features of human baroreflex function. First, the carotid-muscle sympathetic relation is well described by an inverse sigmoid function. Second, a linear relation exists between carotid distending pressure and sympathetic outflow over a range of approximately 25 mmHg. Third, sympathetic responses to changes of carotid pressures are asymmetric; increases of sympathetic activity during carotid compression are much greater than reductions of sympathetic activity during carotid stretch. Fourth, at rest, normal subjects operate near the threshold level for sympathetic excitation. Thus the carotid-muscle sympathetic baroreflex is poised to oppose reductions more effectively than elevations of arterial pressure, and the range of pressures over which the reflex is active is wider than thought hitherto.

  7. Sympathetic nerve in rat with pressure overload left ventricular hypertrophy%瑞舒伐他汀对压力超负荷肥厚大鼠心脏结构和交感神经重构的影响

    Institute of Scientific and Technical Information of China (English)

    廖颖; 曲秀芬; 刘丽; 董兴模; 尹德春

    2009-01-01

    Objective To explore the remodeling mechanism of myocardium and sympathetic nerve in pressure overload left ventricular hypertrophy and elucidate the protective effect of statins. Methods Pressure-overload left ventricular hypertrophy (LVH) of rats was induced by partial coarctation of abdominal aorta; a sham-operated group served as the control (SHAM, n=22). At 8 weeks pest-operation, the animals were divided into two groups and a 12-week treatment period was investigated. At the end of treatment period, eehocardiographic evaluations and hemodynamic measurements were performed. Sympathetic innervation was investigated by analyzing nerve growth factor (NGF), growth associated protein-43 (GAP43) and tyrosine hydroxylase (TH). Results In LVH rats, a significant increase of left ventricular weight, left ventricular weight/body weight, echocardiographic left ventricular end-diastolic diameter, interventricular septum thickness, posterior left ventricular wall thickness, left ventricular systolic pressure and dP/dt was observed. The expressions of NGF and GAP43 protein were significantly down-regulated (0.82±0.06 vs 1.53±0.10, 0.68±0.06 vs 0.81±0.10) and TH level was up-regulated (0.44±0.10 vs 0.62±0.06) by RSV treatment. Conclusion A HMG CoA inhibitor reverses the development of left ventrieular hypertrophy and inhibits sympathetic innervation in abdominal aortic-clamped animals.%目的 探讨大鼠肥厚心肌结构重构、交感神经重构机制及他汀药物的保护作用.方法 62只雄性Wistar大鼠行腹主动脉缩窄术,8周造成压力超负荷性心肌肥厚模型,分为肥厚组和瑞舒伐他汀组,另设22只作为假手术组.瑞舒伐他汀组灌胃给药(10 mg·kg-1·d-1)连续12周后进行超声心动图和血流动力学指标测定.免疫组化法测定心肌中酪氨酸羟化酶(TH)和生长相关因子43(GAP43),Western印迹法检测心肌的TH、GAP43和神经生长因子(NGF)表达水平.结果 (1)肥厚组左室重量(LVW)、左室

  8. 交感神经刺激对周围神经功能影响的实验研究%An experimental study on the effect of electrostimulation of the sympathetic nerve on peripheral nerve function

    Institute of Scientific and Technical Information of China (English)

    沙轲; 陈德松; 朱艺; 陈琳; 彭峰; 方有生

    2006-01-01

    目的观察交感神经兴奋对周围神经电生理和传导功能的影响,探讨颈交感神经兴奋在颈肩痛的发病机制中的可能作用.方法用不同强度电流刺激大鼠颈交感神经后,用肌电图分别检测正中神经神经传导速度(nerve conduction velocity ,NCV)和潜伏期(latency ,LAT).结果电刺激大鼠颈交感神经能降低实验侧正中神经NCV,并使LAT延长,强度越大,NCV和LAT的变化越明显,差异有统计学意义(P<0.05).结论颈交感神经干受刺激可显著地降低其支配的周围神经的功能.周围神经功能降低程度与颈交感神经受刺激强度存在相关关系.

  9. Morphology of sympathetic chain in Saguinus niger

    Directory of Open Access Journals (Sweden)

    MARINA P.E. PINTO

    2013-03-01

    Full Text Available Saguinus niger popularly known as Sauim, is a Brazilian North primate. Sympathetic chain investigation would support traumatic and/or cancer diagnosis which are little described in wild animals. The aim of this study was to describe the morphology and distribution of sympathetic chain in order to supply knowledge for neurocomparative research. Three female young animals that came death by natural causes were investigated. Animals were fixed in formaldehyde 10% and dissected along the sympathetic chain in neck, thorax and abdomen. Cranial cervical ganglion was located at the level of carotid bifurcation, related to carotid internal artery. In neck basis the vagosympathetic trunk divides into the sympathetic trunk and the parasympathetic vagal nerve. Sympathetic trunk ran in dorsal position and originated the stellate ganglia, formed by the fusion of caudal cervical and first thoracic ganglia. Vagal trunk laid ventrally to heart and formed the cardiac plexus. In abdomen, on the right side, were found the celiac ganglion and cranial mesenteric ganglion; in the left side these ganglia were fusioned into the celiac-mesenteric ganglion displaced closely to the celiac artery. In both sides, the caudal mesenteric ganglion was located near to the caudal mesenteric artery.

  10. CT引导下腰交感神经调制治疗女性会阴及下肢多汗症17例疗效观察%Effects of lumbar sympathetic nerve modulation guided by computed tomography for treating female pelvic limb hyperhidrosis

    Institute of Scientific and Technical Information of China (English)

    杨晓敏; 黄冰; 姚明; 周煦燕; 陆雅萍; 过建国; 孙延豹

    2014-01-01

    对17例女性会阴、下肢多汗症患者,在CT引导下经第2、3腰椎(L2~3)间隙穿刺,直至针尖抵达L2或L3椎体前外侧、腰大肌前方,注入含造影剂碘海醇的1%利多卡因液3 ml,观察药液分布在腰大肌与椎体之间,15 min后每侧注入无水酒精5 ml,5 min后脚趾末梢灌注指数上升了(5.9±1.4)倍、双脚掌温上升了(4.16 ±0.89)℃.术后会阴下肢多汗现象消失,半年内均有效,一年内复发1例,无相关并发症发生.提示CT引导下腰交感神经调制治疗女性会阴、下肢多汗症切实、可行.%A total of 17 cases with pelvic limb hyperhidrosis were selected for lumbar sympathetic nerve modulation.The puncture of lumbar sympathetic nerve was guided by computed tomography (CT) through the gap of L2-3 until the needle tip reached the lateral of the second or third lumbar vertebra body and outside of psoas major.A mixture of 1% lidocaine 3 ml and 30% Iohexol injection 0.3 ml was injected.If the diffusion of lidocaine was observed between lumbar vertebra body and psoas major.After 15 min,5 ml of absolute alcohol was injected to modulate the lumbar sympathetic nerve.After 5 min,oximetry-derived perfusion index of toe and sole temperature increased (5.9 ± 1.4) folds and (4.16± 0.89) ℃ on average respectively.Pelvic limb hyperhidrosis was all cured within 6 months and one case recurred after a year.There were no occurrences of complications.Lumbar sympathetic nerve modulation guided by CT may be used for treating female pelvic limbs hyperhidrosis.

  11. Effects of Intrinsic and Extrinsic Cardiac Nerves on Atrial Arrhythmia in Experimental Pulmonary Artery Hypertension.

    Science.gov (United States)

    Zhao, Qingyan; Deng, Hongping; Jiang, Xuejun; Dai, Zixuan; Wang, Xiaozhan; Wang, Xule; Guo, Zongwen; Hu, Wei; Yu, Shengbo; Yang, Bo; Tang, Yanhong; Huang, Congxin

    2015-11-01

    Atrial arrhythmia, which includes atrial fibrillation (AF) and atrial flutter (AFL), is common in patients with pulmonary arterial hypertension (PAH), who often have increased sympathetic nerve activity. Here, we tested the hypothesis that autonomic nerves play important roles in vulnerability to AF/AFL in PAH. The atrial effective refractory period and AF/AFL inducibility at baseline and after anterior right ganglionated plexi ablation were determined during left stellate ganglion stimulation or left renal sympathetic nerve stimulation in beagle dogs with or without PAH. Then, sympathetic nerve, β-adrenergic receptor densities and connexin 43 expression in atrial tissues were assessed. The sum of the window of vulnerability to AF/AFL was increased in the right atrium compared with the left atrium at baseline in the PAH dogs but not in the controls. The atrial effective refractory period dispersion was increased in the control dogs, but not in the PAH dogs, during left stellate ganglion stimulation. The voltage thresholds for inducing AF/AFL during anterior right ganglionated plexi stimulation were lower in the PAH dogs than in the controls. The AF/AFL inducibility was suppressed after ablation of the anterior right ganglionated plexi in the PAH dogs. The PAH dogs had higher sympathetic nerve and β1-adrenergic receptor densities, increased levels of nonphosphorylated connexin 43, and heterogeneous connexin 43 expression in the right atrium when compared with the control dogs. The anterior right ganglionated plexi play important roles in the induction of AF/AFL. AF/AFL induction was associated with right atrium substrate remodeling in dogs with PAH.

  12. EP3 receptors mediate PGE2-induced hypothalamic paraventricular nucleus excitation and sympathetic activation

    Science.gov (United States)

    Zhang, Zhi-Hua; Yu, Yang; Wei, Shun-Guang; Nakamura, Yoshiko; Nakamura, Kazuhiro

    2011-01-01

    Prostaglandin E2 (PGE2), an important mediator of the inflammatory response, acts centrally to elicit sympathetic excitation. PGE2 acts on at least four E-class prostanoid (EP) receptors known as EP1, EP2, EP3, and EP4. Since PGE2 production within the brain is ubiquitous, the different functions of PGE2 depend on the expression of these prostanoid receptors in specific brain areas. The type(s) and location(s) of the EP receptors that mediate sympathetic responses to central PGE2 remain unknown. We examined this question using PGE2, the relatively selective EP receptor agonists misoprostol and sulprostone, and the available selective antagonists for EP1, EP3, and EP4. In urethane-anesthetized rats, intracerebroventricular (ICV) administration of PGE2, sulprostone or misoprostol increased renal sympathetic nerve activity, blood pressure, and heart rate. These responses were significantly reduced by ICV pretreatment with the EP3 receptor antagonist; the EP1 and EP4 receptor antagonists had little or no effect. ICV PGE2 or misoprostol increased the discharge of neurons in the hypothalamic paraventricular nucleus (PVN). ICV misoprostol increased the c-Fos immunoreactivity of PVN neurons, an effect that was substantially reduced by the EP3 receptor antagonist. Real-time PCR detected EP3 receptor mRNA in PVN, and immunohistochemical studies revealed sparsely distributed EP3 receptors localized in GABAergic terminals and on a few PVN neurons. Direct bilateral PVN microinjections of PGE2 or sulprostone elicited sympathoexcitatory responses that were significantly reduced by the EP3 receptor antagonist. These data suggest that EP3 receptors mediate the central excitatory effects of PGE2 on PVN neurons and sympathetic discharge. PMID:21803943

  13. PM2.5对大鼠心脏交感神经分布的影响及其与心肌神经生长因子表达的关系%Effect of PM2.5 on sympathetic innervation by stimulating the secretion of cardiac nerve growth factor in healthy rat hearts

    Institute of Scientific and Technical Information of China (English)

    段军; 丛鲁红; 李刚; 易丽; 柯元南; 周益锋

    2012-01-01

    Objective To assess the effect of PM2.5 on sympathetic innervation and the relationship with cardiac nerve growth factor in healthy rat hearts,identify the ability to the sympathetic nerve reconstruction,and explore the possible arrhythogenic mechanism of PM2.5.Methods Forty healthy SD rats were instilled into trachea with two different solutions twice per week for four weeks:control group with saline and experimental group with PM2.5 25 mg/kg.Then these rats were killed,and biatrial appendages,two ventricular anterior walls were left.Immune cytochemical staining of cardiac nerves was performed using anti-tyrosine hydroxylase antibodies and cardiac nerve growth factor was detected by western blotting.Resuits Compared with the control group,both the density of sympathetic nerves and the expression of cardiac NGF protein in the experimental group were much higher in the left ventricular anterior wall ( P<0.01 and P<0.05) and in the right ventricular anterior wall ( P<0.01 and P<0.05).Conclusions PM2.5 can induce regional sympathetic hyperinnervation in both ventricular anterior walls in healthy rats by stimulating the NGF protein secretion,and the sympathetic nerve reconstruction effect of PM2.5 was confirmed.%目的 研究可吸入颗粒物PM2.5对大鼠心脏交感神经分布的影响及其与心肌神经生长因子表达的关系,明确PM2.5是否具有致交感神经重构作用,探讨PM2.5致心律失常的可能机制.方法 40只SD雄性大鼠,随机分为对照组和实验组,每组20只.实验组大鼠按25 mg/kg剂量经气管内缓慢注入颗粒物悬液染毒,每周染毒2次,连续染毒4周;对照组以生理盐水代替颗粒物悬液;两组大鼠于末次染毒后次日处死,开胸留取双侧心耳和双心室前壁,通过免疫组化方法检测酪氨酸羟化酶染色阳性的交感神经纤维分布密度,同时采用蛋白免疫印迹法检测心肌神经生长因子(NGF)蛋白表达.结果 与对照组比较,实验组大鼠吸入PM2

  14. The articulo-cardiac sympathetic reflex in spinalized, anesthetized rats.

    Science.gov (United States)

    Nakayama, Tomohiro; Suzuki, Atsuko; Ito, Ryuzo

    2006-04-01

    Somatic afferent regulation of heart rate by noxious knee joint stimulation has been proven in anesthetized cats to be a reflex response whose reflex center is in the brain and whose efferent arc is a cardiac sympathetic nerve. In the present study we examined whether articular stimulation could influence heart rate by this efferent sympathetic pathway in spinalized rats. In central nervous system (CNS)-intact rats, noxious articular movement of either the knee or elbow joint resulted in an increase in cardiac sympathetic nerve activity and heart rate. However, although in acutely spinalized rats a noxious movement of the elbow joint resulted in a significant increase in cardiac sympathetic nerve activity and heart rate, a noxious movement of the knee joint had no such effect and resulted in only a marginal increase in heart rate. Because this marginal increase was abolished by adrenalectomy suggests that it was due to the release of adrenal catecholamines. In conclusion, the spinal cord appears to be capable of mediating, by way of cardiac sympathetic nerves, the propriospinally induced reflex increase in heart rate that follows noxious stimulation of the elbow joint, but not the knee joint.

  15. Renal denervation enhances GABA-ergic input into the PVN leading to blood pressure lowering in chronic kidney disease.

    Science.gov (United States)

    Nishihara, Masaaki; Takesue, Ko; Hirooka, Yoshitaka

    2017-05-01

    Sympathoexcitation plays an important role in the pathogenesis of hypertension in patients with chronic kidney disease (CKD). The paraventricular nucleus of the hypothalamus (PVN) in the brain controls sympathetic outflow through γ-amino butyric acid (GABA)-ergic mechanisms. Renal denervation (RDN) exerts a long-term antihypertensive effect in hypertension with CKD; however, the effects of RDN on sympathetic nerve activity and GABA-ergic modulation in the PVN are not clear. We aimed to elucidate whether RDN modulates sympathetic outflow through GABA-ergic mechanisms in the PVN in hypertensive mice with CKD. In 5/6-nephrectomized male Institute of Cancer Research mice (Nx) at 4 weeks after nephrectomy, systolic blood pressure (SBP) was significantly increased, accompanied by sympathoexcitation. The Nx-mice underwent RDN or sham operation, and the mice were divided into three groups (Control, Nx-Sham, and Nx-RDN). At 2 weeks after RDN, SBP was significantly decreased and urinary sodium excretion was increased in Nx-RDN compared with Nx-Sham. Urinary norepinephrine excretion (uNE) levels did not differ significantly between Nx-RDN and Nx-Sham. At 6 weeks after RDN, SBP continued to decrease and uNE levels also decreased in Nx-RDN compared with Nx-Sham. Bicuculline microinjection into the PVN increased mean arterial pressure and lumbar sympathetic nerve activity in all groups. The pressor responses and change in lumbar sympathetic nerve activity were significantly attenuated in Nx-Sham, but were enhanced in Nx-RDN at 6 weeks after RDN. The findings from the present study indicate that RDN has a prolonged antihypertensive effect and, at least in the late phase, decreases sympathetic nerve activity in association with enhanced GABA-ergic input into the PVN in mice with CKD. Copyright © 2016 Elsevier B.V. All rights reserved.

  16. Effect of renal nerve activity on tubular sodium and water reabsorption in dog kidneys as determined by the lithium clearance method

    DEFF Research Database (Denmark)

    Abildgaard, U; Holstein-Rathlou, N H; Leyssac, P P

    1986-01-01

    The reliability of the lithium clearance method in studies of the effect of renal nerve activity upon tubular sodium and water handling in the dog kidney was investigated. Following unilateral acute surgical denervation of the kidney a significant increase in urinary flow rate (40 +/- 7%), sodium...... reabsorption of sodium and water increased significantly by 9 +/- 2% and 8 +/- 2%. Low-frequency electrical stimulation of the distal nerve bundle of the denervated kidney caused a significant decrease in urine flow rate (37 +/- 6%), sodium clearance (31 +/- 4%), lithium clearance (17 +/- 5%) and in fractional...... lithium clearance (18 +/- 5%). Calculated absolute proximal reabsorption rate increased significantly by 17 +/- 3%, while calculated absolute rates of distal sodium and water reabsorption decreased significantly by 16 +/- 5% and 16 +/- 5%. These changes in tubular sodium and water reabsorption during...

  17. 肾交感神经去除术对心力衰竭犬心功能的影响%Influence of renal sympathetic denervation on cardiac function of dogs with heart failure

    Institute of Scientific and Technical Information of China (English)

    黄达民; 侯舒心; 罗晓菡; 张金春; 卢英民

    2016-01-01

    Objective:To study influence of renal sympathetic denervation (RDN)on cardiac function of dogs with heart failure (HF).Methods:A total of 40 dogs were randomly and equally divided into RDN group [received bilat- eral renal artery radiofrequency ablation (RFA)]and model group (only received femoral puncture).Pacemaker was implanted in every dog,and dog HF model was established using rapid right ventricular pacing.Cardiac and re-nal function indexes,BNP and sympathetic activity index levels were observed and compared between two groups be- fore RFA/sham operation,instant and four weeks after model establishment.Results:After operation four weeks, compared with model group,there were significant reductions in levels of epinephrine (E)[(362.69±42.54)ng/ml vs.(290.36±42.32)ng/ml],renin (R)[(305.46± 39.68)ng/ml vs.(230.04±32.80)ng/ml],aldosterone (AD)[(408.00±38.56)ng/ml vs.(246.00± 48.37)ng/ml],angiotensin Ⅱ (ATⅡ)[(280.00±48.08)pg/ml vs.(172.00±25.04)pg/ml]and norepinephrine (NE)[(425.65±50.54)ng/ml vs.(316.76±46.29)ng/ml]in RDN group (P<0.05 all);there were significant reductions in HR,respiratory rate (RR)and BNP level in RDN group,P<0.05 all;there were significant rise in SBP,LVEF,CO,CI,left ventricular pressure maximal rising rate (+dp/dtmax),left ventricular pressure maximal dropping rate (-dp/dtmax)and left ventricular end-systolic pressure (LVESP),and significant reductions in left ventricular end-systolic dimension (LVESd),left ventricular end-diastolic dimension (LVEDd)and left ventricular end-diastolic pressure (LVEDP)in RDN group,P<0.05 all.Conclusion:RDN can decrease renal sympathetic activity,improve heart function,inhibit myocardial remode- ling,its therapeutic effect is significant%目的:研究肾交感神经去除术(RDN)对心力衰竭(HF)犬心功能的影响.方法:选择实验犬40只,随机均分为RDN组(接受双肾动脉射频消融)及模型组(仅予股动脉穿刺).40只犬均安置心脏起搏器,用快速右室起搏的方法

  18. P2 receptors in the central and peripheral nervous systems modulating sympathetic vasomotor tone.

    Science.gov (United States)

    Ralevic, V

    2000-07-01

    Arterial pressure depends on the level of activity of sympathetic vasoconstrictor outflow to blood vessels. This activity is generated in the central nervous system, and involves inputs from a variety of brain regions projecting to sympathetic preganglionic neurones. Of especial interest are a group of neurones in the rostral ventrolateral medulla (RVLM), as they have been demonstrated to have a fundamental role in reflex regulation of the cardiovascular system, and in generation of tonic drive to sympathetic outflow. Sympathetic outflow to blood vessels is additionally modulated at sympathetic ganglia, and at the peripheral terminals of sympathetic nerves. This review considers the role of P2 purine receptors in this neural pathway. Ionotropic P2X receptors are expressed in the RVLM, in sympathetic ganglia, and at the sympathetic neuromuscular junction, and mediate fast excitatory neurotransmission, indicating a general role for ATP as a regulator of sympathetic vasomotor tone. P2Y receptors couple to G proteins and mediate slower signalling to ATP; they have been reported to inhibit prejunctionally neurotransmission at the peripheral terminals of sympathetic nerves, but little is known about their possible role in the central nervous system and in sympathetic ganglia.

  19. Renal neurohormonal regulation in heart failure decompensation.

    Science.gov (United States)

    Jönsson, Sofia; Agic, Mediha Becirovic; Narfström, Fredrik; Melville, Jacqueline M; Hultström, Michael

    2014-09-01

    Decompensation in heart failure occurs when the heart fails to balance venous return with cardiac output, leading to fluid congestion and contributing to mortality. Decompensated heart failure can cause acute kidney injury (AKI), which further increases mortality. Heart failure activates signaling systems that are deleterious to kidneys such as renal sympathetic nerve activity (RSNA), renin-angiotensin-aldosterone system, and vasopressin secretion. All three reduce renal blood flow (RBF) and increase tubular sodium reabsorption, which may increase renal oxygen consumption causing AKI through renal tissue hypoxia. Vasopressin contributes to venous congestion through aquaporin-mediated water retention. Additional water retention may be mediated through vasopressin-induced medullary urea transport and hyaluronan but needs further study. In addition, there are several systems that could protect the kidneys and reduce fluid retention such as natriuretic peptides, prostaglandins, and nitric oxide. However, the effect of natriuretic peptides and nitric oxide are blunted in decompensation, partly due to oxidative stress. This review considers how neurohormonal signaling in heart failure drives fluid retention by the kidneys and thus exacerbates decompensation. It further identifies areas where there is limited data, such as signaling systems 20-HETE, purines, endothelin, the role of renal water retention mechanisms for congestion, and renal hypoxia in AKI during heart failure.

  20. Treating resistant hypertension: role of renal denervation

    Directory of Open Access Journals (Sweden)

    Urban D

    2013-09-01

    Full Text Available Daniel Urban, Sebastian Ewen, Christian Ukena, Dominik Linz, Michael Böhm, Felix Mahfoud Department of Internal Medicine III, Cardiology, Angiology and Intensive Care Medicine, University Hospital of Saarland, Homburg, Saarland, Germany Abstract: Arterial hypertension is the most prevalent risk factor associated with increased cardiovascular morbidity and mortality. Although pharmacological treatment is generally well tolerated, 5%–20% of patients with hypertension are resistant to medical therapy, which is defined as blood pressure above goal (>140/90 mmHg in general; >130–139/80–85 mmHg in patients with diabetes mellitus; >130/80 mmHg in patients with chronic kidney disease despite treatment with ≥3 antihypertensive drugs of different classes, including a diuretic, at optimal doses. These patients are at significantly higher risk for cardiovascular events, in particular stroke, myocardial infarction, and heart failure, as compared with patients with nonresistant hypertension. The etiology of resistant hypertension is multifactorial and a number of risk factors have been identified. In addition, resistant hypertension might be due to secondary causes such as primary aldosteronism, chronic kidney disease, renal artery stenosis, or obstructive sleep apnea. To identify patients with resistant hypertension, the following must be excluded: pseudo-resistance, which might be due to nonadherence to medical treatment; white-coat effect; and inaccurate measurement technique. Activation of the sympathetic nervous system contributes to the development and maintenance of hypertension by increasing renal renin release, decreasing renal blood flow, and enhancing tubular sodium retention. Catheter-based renal denervation (RDN is a novel technique specifically targeting renal sympathetic nerves. Clinical trials have demonstrated that RDN significantly reduces blood pressure in patients with resistant hypertension. Experimental studies and small

  1. Immunopathology of sympathetic ophthalmia.

    Science.gov (United States)

    Marak, G E

    1976-01-01

    The long held notion that sympathetic ophthalmia represents an autoimmune reaction to uveal pigment is no longer tenable. Pigmentation influences the histopathologic picture of sympathetic ophthalmia but no evidence supports the role of uveal pigment as inciting antigen. Several recent studies have confirmed our initial report of the participation of cellular hypersensitivity to ocular tissues in the pathogenesis of this disease. Both clinical and experimental studies implicate retinal tissue as being more immunogenic than uveal antigens. The recent histopathologic observation that eosinophils concentrate near the choriocapillaris suggests that outer retina and retinal pigment epithelium should not be overlooked as a potential source of the stimulating antigen in sympathetic ophthalmia.

  2. Effect of Renal Sympathetic Denervation on Endothelial Function in Hypertensive Dogs%去肾脏交感神经术对犬高血压及内皮功能的研究

    Institute of Scientific and Technical Information of China (English)

    赵斌; 卢成志; 张欣; 于翔; 王彦欧

    2012-01-01

    Objective: To explore the relationship between hypertension, renal sympathetic activity and endothelial function in dogs. Methods: Eighteen mongrel dogs were divided into intervention group (n=10) and control group (n=8). The hypertension model was made in dogs of intervention group. The percutaneous catheter-based radiofrequency was given to dogs in two groups. Values of mean blood pressure (MAP) and angiotensin II (Ang II) were detected before operation and at 2, 4 and 10 weeks after operation. The changes of endothelin-1 (ET-1) and calcitonin gene related peptide (CGRP) were detected before and 12 weeks after molding, and 10 weeks after denervation. ReSUltSrThe values of MAP and Ang II were significantly lower 2, 4 and 10 weeks after operation than those before operation in two groups (P < 0.05 or P < 0.01). The level of ET-1 was higher after 12 weeks in intervention group, but lower after denervation. The level of CGR was significantly lower after 12 weeks in intervention group (P < 0.01), but was significantly increased after denervation (P < 0.01). Conclusion: Renal sympathetic denervation can significantly decrease blood pressure and improve endothelial dysfunction in dogs.%目的:探讨高血压病与交感神经兴奋及内皮功能的关系.方法:18只杂种犬随机分为高血压模型组(n=10)和对照组(n=8).高血压模型组于全身麻醉下手术分离颈动脉和迷走神经后制作高血压模型,对照组同样操作但不制作高血压模型,造模12周后,2组动物都接受去肾脏交感神经术.测量2组术前和术后2、4、10周的平均动脉压(MAP)和血管紧张素Ⅱ(AngⅡ),测量高血压模型组造模前、造模后12周和去神经术后10周的内皮素-1(ET-1)及降钙素基因相关肽(CGRP).结果:2组术后2、4、10周的MAP和AngⅡ均低于术前,差异有统计学意义(P< 0.05或P<0.01).在高血压模型组,造模后12周ET-1水平较造模前升高,去神经术后又下降;CGRP在造模后12周较造模

  3. Contribution of renal innervation to hypertension in rat autosomal dominant polycystic kidney disease.

    Science.gov (United States)

    Gattone, Vincent H; Siqueira, Tibério M; Powell, Charles R; Trambaugh, Chad M; Lingeman, James E; Shalhav, Arieh L

    2008-08-01

    The kidney has both afferent (sensory) and efferent (sympathetic) nerves that can influence renal function. Renal innervation has been shown to play a role in the pathogenesis of many forms of hypertension. Hypertension and flank pain are common clinical manifestations of autosomal dominant (AD) polycystic kidney disease (PKD). We hypothesize that renal innervation contributes to the hypertension and progression of cystic change in rodent PKD. In the present study, the contribution of renal innervation to hypertension and progression of renal histopathology and dysfunction was assessed in male Han:SPRD-Cy/+ rats with ADPKD. At 4 weeks of age, male offspring from crosses of heterozygotes (Cy/+) were randomized into either 1) bilateral surgical renal denervation, 2) surgical sham denervation control, or 3) nonoperated control groups. A midline laparotomy was performed to allow the renal denervation (i.e., physical stripping of the nerves and painting the artery with phenol/alcohol). Blood pressure (tail cuff method), renal function (BUN) and histology were assessed at 8 weeks of age. Bilateral renal denervation reduced the cystic kidney size, cyst volume density, systolic blood pressure, and improved renal function (BUN) as compared with nonoperated controls. Operated control cystic rats had kidney weights, cyst volume densities, systolic blood pressures, and plasma BUN levels that were intermediate between those in the denervated animals and the nonoperated controls. The denervated group had a reduced systolic blood pressure compared with the operated control animals, indicating that the renal innervations was a major contributor to the hypertension in this model of ADPKD. Renal denervation was efficacious in reducing some pathology, including hypertension, renal enlargement, and cystic pathology. However, sham operation also affected the cystic disease but to a lesser extent. We hypothesize that the amelioration of hypertension in Cy/+ rats was due to the effects

  4. Sympathetic Blocks Provided Sustained Pain Relief in a Patient with Refractory Painful Diabetic Neuropathy

    OpenAIRE

    2012-01-01

    The sympathetic nervous system has been implicated in pain associated with painful diabetic neuropathy. However, therapeutic intervention targeted at the sympathetic nervous system has not been established. We thus tested the hypothesis that sympathetic nerve blocks significantly reduce pain in a patient with painful diabetic neuropathy who has failed multiple pharmacological treatments. The diagnosis of small fiber sensory neuropathy was based on clinical presentations and confirmed by skin ...

  5. Role of sympathetic nervous system and neuropeptides in obesity hypertension

    Directory of Open Access Journals (Sweden)

    J.E. Hall

    2000-06-01

    Full Text Available Obesity is the most common cause of human essential hypertension in most industrialized countries. Although the precise mechanisms of obesity hypertension are not fully understood, considerable evidence suggests that excess renal sodium reabsorption and a hypertensive shift of pressure natriuresis play a major role. Sympathetic activation appears to mediate at least part of the obesity-induced sodium retention and hypertension since adrenergic blockade or renal denervation markedly attenuates these changes. Recent observations suggest that leptin and its multiple interactions with neuropeptides in the hypothalamus may link excess weight gain with increased sympathetic activity. Leptin is produced mainly in adipocytes and is believed to regulate energy balance by acting on the hypothalamus to reduce food intake and to increase energy expenditure via sympathetic activation. Short-term administration of leptin into the cerebral ventricles increases renal sympathetic activity, and long-term leptin infusion at rates that mimic plasma concentrations found in obesity raises arterial pressure and heart rate via adrenergic activation in non-obese rodents. Transgenic mice overexpressing leptin also develop hypertension. Acute studies suggest that the renal sympathetic effects of leptin may depend on interactions with other neurochemical pathways in the hypothalamus, including the melanocortin-4 receptor (MC4-R. However, the role of this pathway in mediating the long-term effects of leptin on blood pressure is unclear. Also, it is uncertain whether there is resistance to the chronic renal sympathetic and blood pressure effects of leptin in obese subjects. In addition, leptin also has other cardiovascular and renal actions, such as stimulation of nitric oxide formation and improvement of insulin sensitivity, which may tend to reduce blood pressure in some conditions. Although the role of these mechanisms in human obesity has not been elucidated, this

  6. The Sympathetic Release Test: A Test Used to Assess Thermoregulation and Autonomic Control of Blood Flow

    Science.gov (United States)

    Tansey, E. A.; Roe, S. M.; Johnson, C. J.

    2014-01-01

    When a subject is heated, the stimulation of temperature-sensitive nerve endings in the skin, and the raising of the central body temperature, results in the reflex release of sympathetic vasoconstrictor tone in the skin of the extremities, causing a measurable temperature increase at the site of release. In the sympathetic release test, the…

  7. The Sympathetic Release Test: A Test Used to Assess Thermoregulation and Autonomic Control of Blood Flow

    Science.gov (United States)

    Tansey, E. A.; Roe, S. M.; Johnson, C. J.

    2014-01-01

    When a subject is heated, the stimulation of temperature-sensitive nerve endings in the skin, and the raising of the central body temperature, results in the reflex release of sympathetic vasoconstrictor tone in the skin of the extremities, causing a measurable temperature increase at the site of release. In the sympathetic release test, the…

  8. Reduced sympathetic nervous activity. A potential mechanism predisposing to body weight gain.

    OpenAIRE

    Spraul, M; Ravussin, E; Fontvieille, A M; Rising, R; Larson, D. E.; Anderson, E A

    1993-01-01

    The sympathetic nervous system is recognized to play a role in the etiology of animal and possibly human obesity through its impact on energy expenditure and/or food intake. We, therefore, measured fasting muscle sympathetic nerve activity (MSNA) in the peroneal nerve and its relationship with energy expenditure and body composition in 25 relatively lean Pima Indian males (means +/- SD; 26 +/- 6 yr, 82 +/- 19 kg, 28 +/- 10% body fat) and 19 Caucasian males (29 +/- 5 yr, 81 +/- 13 kg, 24 +/- 9...

  9. CT引导下经皮穿刺胸交感链阻滞治疗手汗症的临床效果%Therapeutic feasibility of percutaneous puncture and chemical neurolysis of thoracic sympathetic nerve block in palmar hyperhidrosis under the guidance of computed tomograph

    Institute of Scientific and Technical Information of China (English)

    黄冰; 姚明; 周煦燕; 曹浩强; 祝则峰; 侯健; 陆雅萍; 孙建良; 胡奕

    2011-01-01

    Objective To explore the therapeutic feasibility of percutaneous puncture and neurolytic thoracic sympathetic nerve block under the guidance of computed tomograph (CT).Methods From September 2009 to August 2010,23 cases with primary palmar hyperhidrosis underwent percutaneous puncture and neurolytic thoracic sympathetic nerve block at our hospital.The puncture of thoracic sympathetic nerve was guided by CT through the gap of T3-4.The screen showed the direction of needle and the location of needle tip at the upper joint of costal head beside T3 body and outside of costal pleura.A mixed injection of 1% lidocaine and 30% iohexol was administered.On CT,lidocaine was found to cover the area where the thoracic sympathetic nerve was located.And after several minutes,the patient's palms turned warm and dry from cool and wet without the onset of Homer's syndrome.Then 2.5 ml of absolute alcohol was injected to block the thoracic sympathetic nerve.Results CT could guide the needle to the right position.And the injectate spreaded to the site of thoracic sympathetic nerve.At 5 min after anesthetic injection,the palmar temperature raised an average of 2.86 ℃ and the amplitude of pulse rose over 55%.Palmar hyperhidrosis was cured in 19 patients by one attempt and 4 patients required a second block with absolute alcohol.No complication occurred and there were 2 patients with tendency of recurrence during a follow-up period of 8 - 18 months.Conclusion The CT-guided therapy of percutaneous puncture and chemical neurolysis of thoracic sympathetic nerve block is both feasible and efficacious for palmar hyperhidrosis.%目的 探讨CT引导下经皮穿刺胸交感神经阻滞治疗手汗症的可行性.方法 2009年10月至2010年8月间在浙江省嘉兴市第一医院接受CT引导下经皮穿刺胸交感神经阻滞治疗的原发性手汗症患者23例,在CT引导下经胸3/4( T3/4)椎间隙穿刺,直至针尖解剖定位于第4肋骨小头上缘、第3椎体旁的壁胸

  10. Differential activation of sympathetic discharge to skin and skeletal muscle in humans.

    Science.gov (United States)

    Vissing, S F

    1997-01-01

    The present work provides insight into the relative contribution of different mechanisms in regulating sympathetic discharge to skin and skeletal muscle in humans. Activation of sympathetic nerve activity during common behaviours such as orthostasis and exercise was shown to be highly selective, depending on the specific sympathetic outflow under study. Regarding orthostasis, data from experiments in this thesis revoked the concept that cardiopulmonary afferents only regulate muscle vascular resistance in the forearm, not in the leg. Also the concept that the cutaneous circulation is under baroreceptor control has been challenged. Unloading cardiopulmonary afferents with lower body negative pressure elicited intensity dependent increases in peroneal sympathetic discharge to skeletal muscle, and increases in forearm and calf vascular resistances. Therefore, it was concluded that cardiopulmonary afferents regulate vascular resistance in skeletal muscle of both forearm and calf, suggesting an important role for these afferents in the reflex adjustments to upright posture. In contrast to muscle sympathetic nerve activity, baroreceptor deactivation with lower body negative pressure had no effect on skin sympathetic nerve activity or skin vascular resistance. However, assumption of upright posture increased skin vascular resistance, this increase was abolished when increased vascular transmural pressure was avoided by elevating the arm. Local cutaneous nerve blockade, but not blockade of efferent sympathetic nerve traffic, abolished the vasoconstrictor response to upright posture. Based on these experiments, it was concluded that baroreceptor afferents do not regulate sympathetic vasoconstrictor outflow to the cutaneous circulation. During upright posture at normothermia cutaneous vasoconstriction is mainly driven by a local reflex. To explain activation of sympathetic outflow during exercise two theories have been proposed. One is that a "central motor command" signal

  11. Menstrual cycle effects on sympathetic neural responses to upright tilt.

    NARCIS (Netherlands)

    Fu, Q.; Okazaki, K.; Shibata, S.; Shook, R.P.; Gunday, T.B. van; Galbreath, M.M.; Reelick, M.F; Levine, B.D.

    2009-01-01

    Young women are more susceptible to orthostatic intolerance than men, though the sex-specific pathophysiology remains unknown. As blood pressure (BP) is regulated through the baroreflex mechanism, we tested the hypothesis that baroreflex control of muscle sympathetic nerve activity (MSNA) during

  12. [Peripheral nerve injuries complicating extracranial vascular surgery (author's transl)].

    Science.gov (United States)

    Grobe, T; Raithel, D

    1978-10-01

    Peripheral nerve injuries may complicate extracranial vascular surgery. Pareses of the recurrent and hypoglossal nerves are clinically important. The nervus laryngeus superior, the ramus marginalis mandibulae of the facial nerve and the brachial plexus may be involved. Horner's syndrom indicating damage of sympathetic fibers may also appear. Lesions of the glossopharyngeal, vagus and phrenic nerves are rather seldom.

  13. Renal dopamine receptors and hypertension.

    Science.gov (United States)

    Hussain, Tahir; Lokhandwala, Mustafa F

    2003-02-01

    Dopamine has been recognized as an important modulator of central as well as peripheral physiologic functions in both humans and animals. Dopamine receptors have been identified in a number of organs and tissues, which include several regions within the central nervous system, sympathetic ganglia and postganglionic nerve terminals, various vascular beds, the heart, the gastrointestinal tract, and the kidney. The peripheral dopamine receptors influence cardiovascular and renal function by decreasing afterload and vascular resistance and promoting sodium excretion. Within the kidney, dopamine receptors are present along the nephron, with highest density on proximal tubule epithelial cells. It has been reported that there is a defective dopamine receptor, especially D(1) receptor function, in the proximal tubule of various animal models of hypertension as well as in humans with essential hypertension. Recent reports have revealed the site of and the molecular mechanisms responsible for the defect in D(1) receptors in hypertension. Moreover, recent studies have also demonstrated that the disruption of various dopamine receptor subtypes and their function produces hypertension in rodents. In this review, we present evidence that dopamine and dopamine receptors play an important role in regulating renal sodium excretion and that defective renal dopamine production and/or dopamine receptor function may contribute to the development of various forms of hypertension.

  14. Bursting into space: alterations of sympathetic control by space travel

    Science.gov (United States)

    Eckberg, D. L.

    2003-01-01

    AIM: Astronauts return to Earth with reduced red cell masses and hypovolaemia. Not surprisingly, when they stand, their heart rates may speed inordinately, their blood pressures may fall, and some may experience frank syncope. We studied autonomic function in six male astronauts (average +/- SEM age: 40 +/- 2 years) before, during, and after the 16-day Neurolab space shuttle mission. METHOD: We recorded electrocardiograms, finger photoplethysmographic arterial pressures, respiration, peroneal nerve muscle sympathetic activity, plasma noradrenaline and noradrenaline kinetics, and cardiac output, and we calculated stroke volume and total peripheral resistance. We perturbed autonomic function before and during spaceflight with graded Valsalva manoeuvres and lower body suction, and before and after the mission with passive upright tilt. RESULTS: In-flight baseline sympathetic nerve activity was increased above pre-flight levels (by 10-33%) in three subjects, in whom noradrenaline spillover and clearance also were increased. Valsalva straining provoked greater reductions of arterial pressure, and proportionally greater sympathetic responses in space than on Earth. Lower body suction elicited greater increases of sympathetic nerve activity, plasma noradrenaline, and noradrenaline spillover in space than on Earth. After the Neurolab mission, left ventricular stroke volume was lower and heart rate was higher during tilt, than before spaceflight. No astronaut experienced orthostatic hypotension or pre-syncope during 10 min of post-flight tilting. CONCLUSION: We conclude that baseline sympathetic outflow, however measured, is higher in space than on earth, and that augmented sympathetic nerve responses to Valsalva straining, lower body suction, and post-flight upright tilt represent normal adjustments to greater haemodynamic stresses associated with hypovolaemia.

  15. Obesity-Related Metabolic Syndrome: Mechanisms of Sympathetic Overactivity

    Directory of Open Access Journals (Sweden)

    Maria Paola Canale

    2013-01-01

    Full Text Available The prevalence of the metabolic syndrome has increased worldwide over the past few years. Sympathetic nervous system overactivity is a key mechanism leading to hypertension in patients with the metabolic syndrome. Sympathetic activation can be triggered by reflex mechanisms as arterial baroreceptor impairment, by metabolic factors as insulin resistance, and by dysregulated adipokine production and secretion from visceral fat with a mainly permissive role of leptin and antagonist role of adiponectin. Chronic sympathetic nervous system overactivity contributes to a further decline of insulin sensitivity and creates a vicious circle that may contribute to the development of hypertension and of the metabolic syndrome and favor cardiovascular and kidney disease. Selective renal denervation is an emerging area of interest in the clinical management of obesity-related hypertension. This review focuses on current understanding of some mechanisms through which sympathetic overactivity may be interlaced to the metabolic syndrome, with particular regard to the role of insulin resistance and of some adipokines.

  16. Sympathetic adaptations to one-legged training

    Science.gov (United States)

    Ray, C. A.

    1999-01-01

    The purpose of the present study was to determine the effect of leg exercise training on sympathetic nerve responses at rest and during dynamic exercise. Six men were trained by using high-intensity interval and prolonged continuous one-legged cycling 4 day/wk, 40 min/day, for 6 wk. Heart rate, mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA; peroneal nerve) were measured during 3 min of upright dynamic one-legged knee extensions at 40 W before and after training. After training, peak oxygen uptake in the trained leg increased 19 +/- 2% (P training (108 +/- 5 to 96 +/- 5 beats/min and 132 +/- 8 to 119 +/- 4 mmHg, respectively, during the third minute of exercise; P training. However, MSNA was significantly less during the third minute of exercise after training (32 +/- 2 to 22 +/- 3 bursts/min; P training effect on MSNA remained when MSNA was expressed as bursts per 100 heartbeats. Responses to exercise in five untrained control subjects were not different at 0 and 6 wk. These results demonstrate that exercise training prolongs the decrease in MSNA during upright leg exercise and indicates that attenuation of MSNA to exercise reported with forearm training also occurs with leg training.

  17. Regional sympathetic denervation after myocardial infarction in humans detected noninvasively using I-123-metaiodobenzylguanidine

    Energy Technology Data Exchange (ETDEWEB)

    Stanton, M.S.; Tuli, M.M.; Radtke, N.L.; Heger, J.J.; Miles, W.M.; Mock, B.H.; Burt, R.W.; Wellman, H.N.; Zipes, D.P. (Indiana Univ. School of Medicine, IN (USA))

    1989-11-15

    Transmural myocardial infarction in dogs produces denervation of sympathetic nerves in viable myocardium apical to the infarct that may be arrhythmogenic. It is unknown whether sympathetic denervation occurs in humans. The purpose of this study was to use iodine-123-metaiodobenzylguanidine (MIBG), a radiolabeled guanethidine analog that is actively taken up by sympathetic nerve terminals, to image noninvasively the cardiac sympathetic nerves in patients with and without ventricular arrhythmias after myocardial infarction. Results showed that 10 of 12 patients with spontaneous ventricular tachyarrhythmias after myocardial infarction exhibited regions of thallium-201 uptake indicating viable perfused myocardium, with no MIBG uptake. Such a finding is consistent with sympathetic denervation. One patient had frequent episodes of nonsustained ventricular tachycardia induced at exercise testing that was eliminated by beta-adrenoceptor blockade. Eleven of the 12 patients had ventricular tachycardia induced at electrophysiologic study and metoprolol never prevented induction. Sympathetic denervation was also detected in two of seven postinfarction patients without ventricular arrhythmias. Normal control subjects had no regions lacking MIBG uptake. This study provides evidence that regional sympathetic denervation occurs in humans after myocardial infarction and can be detected noninvasively by comparing MIBG and thallium-201 images. Although the presence of sympathetic denervation may be related to the onset of spontaneous ventricular tachyarrhythmias in some patients, it does not appear to be related to sustained ventricular tachycardia induced at electrophysiologic study.

  18. A novel electrophilic synthesis and evaluation of medium specific radioactivity (1R,2S)-4-[{sup 18}F]fluorometaraminol, a tracer for the assessment of cardiac sympathetic nerve integrity with PET

    Energy Technology Data Exchange (ETDEWEB)

    Eskola, Olli E-mail: olesko@utu.fi; Groenroos, Tove; Bergman, Joergen; Haaparanta, Merja; Marjamaeki, Paeivi; Lehikoinen, Pertti; Forsback, Sarita; Langer, Oliver; Hinnen, Francoise; Dolle, Frederic; Halldin, Christer; Solin, Olof

    2004-01-01

    (1R,2S)-4-[{sup 18}F]fluorometaraminol (4-[{sup 18}F]FMR), a tracer for cardiac sympathetic innervation, was synthesized by electrophilic aromatic substitution. A trimethylstannyl precursor, protected with tert-butoxycarbonyl protecting groups, was radiofluorinated with high specific radioactivity [{sup 18}F]F{sub 2}. Specific radioactivity of 4-[{sup 18}F]FMR, in average 11.8 {+-}3.3 GBq/{mu}mol, was improved 40-800-fold in comparison to the previous electrophilic fluorinations. The biodistribution of 4-[{sup 18}F]FMR in rat was in accordance with the known distribution of sympathetic innervation. 4-[{sup 18}F]FMR showed no metabolic degradation in left ventricle of rat heart, where the uptake was high, rapid and specific.

  19. Surgical anatomy of the retroperitoneal spaces, Part IV: retroperitoneal nerves.

    Science.gov (United States)

    Mirilas, Petros; Skandalakis, John E

    2010-03-01

    We present surgicoanatomical topographic relations of nerves and plexuses in the retroperitoneal space: 1) six named parietal nerves, branches of the lumbar plexus: iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, obturator, femoral. 2) The sacral plexus is formed by the lumbosacral trunk, ventral rami of S1-S3, and part of S4; the remainder of S4 joining the coccygeal plexus. From this plexus originate the superior gluteal nerve, which passes backward through the greater sciatic foramen above the piriformis muscle; the inferior gluteal nerve also courses through the greater sciatic foramen, but below the piriformis; 3) sympathetic trunks: right and left lumbar sympathetic trunks, which comprise four interconnected ganglia, and the pelvic chains; 4) greater, lesser, and least thoracic splanchnic nerves (sympathetic), which pass the diaphragm and join celiac ganglia; 5) four lumbar splanchnic nerves (sympathetic), which arise from lumbar sympathetic ganglia; 6) pelvic splanchnic nerves (nervi erigentes), providing parasympathetic innervation to the descending colon and pelvic splanchna; and 7) autonomic (prevertebral) plexuses, formed by the vagus nerves, splanchnic nerves, and ganglia (celiac, superior mesenteric, aorticorenal). They include sympathetic, parasympathetic, and sensory (mainly pain) fibers. The autonomic plexuses comprise named parts: aortic, superior mesenteric, inferior mesenteric, superior hypogastric, and inferior hypogastric (hypogastric nerves).

  20. Cervical vagus and sympathetic trunk and fiber components of external laryngeal nerve: comparative anatomy between human and dog%人与狗迷走/交感干的比较解剖及其喉上神经外支纤维成分

    Institute of Scientific and Technical Information of China (English)

    许士叶; 董剑平; 孙善全; Kannaiyan Vijesh Ramnarayan; Joyeeta Sengupta

    2012-01-01

    目的 对人与狗的颈段迷走/交感干进行比较解剖,并鉴定狗的喉上神经外支的纤维成分.方法 随机解剖经福尔马林固定的成年人尸体颈部(n=50)及狗的颈部(n=10),暴露其颈交感干与喉上神经及其外支间的交通;并取狗的喉上神经外支,甲醛固定,明胶包埋,恒冷切片后用Kamovsky AchE组化方法染色并观察.结果 狗的迷走神经结状神经节与颈上神经节完全或部分融合,迷走神经干与交感神经干完全或部分融合为迷走-交感干;而人的结状神经节与颈上神经节互相分离;颈上神经节与喉上神经及其分支之间存在交通,其中颈上神经节与喉上神经外支相交通者占86%.AchE染色显示:狗的喉上神经外支含AchE阳性有髓神经纤维、AchE阴性有髓神经纤维和AchE阳性无髓神经纤维. 结论 喉上神经外支呈袢状,而非干式,含躯体运动、交感神经节后及躯体感觉纤维,因此喉上神经外支为一混合神经.%Objective To compare the differences of cervical vagus and sympathetic trunks between human being and dog, and identify the fiber components of the dog external laryngeal nerve (ELN). Methods SO adult human cadavers fixed with formalin and 10 fresh dog cadavers were randomly used. The superior laryngeal nerve and its branches, superior cervical sympathetic ganglion (SCSG) and nodose ganglion (NG) were exposed. The communications between the cervical sympathetic trunk and the superior laryngeal nerve (SLN) were identified. The tissues from ELN and NG together with a branch from dog SCSG were taken for AchE activity analysis. Results In dog, the nodosum of vagus and the SCSG were completely or partially fused. In human being, the nodosum of vagus and SCSG separated, and in the most cases (86%) the SCSG connected with the ELN. The AchE staining demonstrated the presence of three different types of fibers in dog ELN: AchE-positive myelinated fibers, AchE-negative myelinated fibers and Ach

  1. Interaction of Xylamine with peripheral sympathetic neurons

    Energy Technology Data Exchange (ETDEWEB)

    Ransom, R.W.; Waggaman, L.A.; Cho, A.K.

    1985-09-30

    Xylamine (XYL) administered to intact rats caused a 70-80% reduction in norepinephrine (NE) uptake by the vas deferens but had little or no effect on NE content in that tissue. The vas deferens accumulates /sup 3/H-XYL in vitro by a desmethylimipramine (DMI)-sensitive mechanism. Vasa deferentia from 6-hydroxydopamine (60HDA) pretreated animals exhibited a 80% reduction in both NE content and XYL uptake activity. These results indicate that XYL is taken up by sympathetic nerve terminals and can reduce NE uptake activity without depleting terminals of neurotransmitter. 9 references, 4 tables.

  2. Cervical sympathetic chain schwannoma: A case report

    Directory of Open Access Journals (Sweden)

    Inès Nacef

    2014-07-01

    Full Text Available Nerve tumors arising from the sympathetic chain are uncommon slow-growing tumors and represent a diagnosis challenge. Their malignant degeneration is rare. Definitive pre-operative diagnosis may be difficult as investigations are not usually helpful. We report the case of a 23-year old woman who presented with an asymptomatic solitary left cervical swelling. She was evaluated with sonography and computed tomography. Complete surgical excision of the lesion was carried out and histologic examination revealed a schwannoma. Post-operatively, the patient showed clinical findings of Horner’s syndrome. Pathologic and radiological evaluation, differential diagnosis of this neoplasm and its management are discussed.

  3. Pediatric cervical sympathetic chain schwannoma with Horner syndrome: a rare case presentation.

    Science.gov (United States)

    Bhagat, Sanjeev; Varshney, Saurabh; Bist, Sampan S; Gupta, Nitin

    2014-03-01

    Schwannomas are rare, benign, slowly growing neurogenic tumors that originate in peripheral, spinal, or cranial nerves other than the optic and olfactory nerves. In the head and neck, these tumors usually arise from the vagus nerve and the cervical sympathetic chain in the parapharyngeal space. Cervical sympathetic chain schwannomas represent a rare subgroup of schwannomas; fewer than 60 cases have been reported in the literature. These tumors are rarely seen in children and adolescents. Because patients typically present with an asymptomatic neck mass and vague complaints, clinical suspicion is important in making the diagnosis. Neural deficits at presentation are uncommon. The presence of features of Horner syndrome before excision is very rare, having been previously reported in only 10 cases of cervical sympathetic chain schwannoma. We report an extremely rare case of a cervical sympathetic chain schwannoma in a child who presented with Horner syndrome. The lesion was successfully excised.

  4. Sympathetic neuro-adipose connections mediate leptin-driven lipolysis.

    Science.gov (United States)

    Zeng, Wenwen; Pirzgalska, Roksana M; Pereira, Mafalda M A; Kubasova, Nadiya; Barateiro, Andreia; Seixas, Elsa; Lu, Yi-Hsueh; Kozlova, Albina; Voss, Henning; Martins, Gabriel G; Friedman, Jeffrey M; Domingos, Ana I

    2015-09-24

    Leptin is a hormone produced by the adipose tissue that acts in the brain, stimulating white fat breakdown. We find that the lipolytic effect of leptin is mediated through the action of sympathetic nerve fibers that innervate the adipose tissue. Using intravital two-photon microscopy, we observe that sympathetic nerve fibers establish neuro-adipose junctions, directly "enveloping" adipocytes. Local optogenetic stimulation of sympathetic inputs induces a local lipolytic response and depletion of white adipose mass. Conversely, genetic ablation of sympathetic inputs onto fat pads blocks leptin-stimulated phosphorylation of hormone-sensitive lipase and consequent lipolysis, as do knockouts of dopamine β-hydroxylase, an enzyme required for catecholamine synthesis. Thus, neuro-adipose junctions are necessary and sufficient for the induction of lipolysis in white adipose tissue and are an efferent effector of leptin action. Direct activation of sympathetic inputs to adipose tissues may represent an alternative approach to induce fat loss, circumventing central leptin resistance. PAPERCLIP. Copyright © 2015 Elsevier Inc. All rights reserved.

  5. Cardiac Autonomic Nerve Stimulation in the Treatment of Heart Failure

    OpenAIRE

    Kobayashi, Mariko; Massiello, Alex; Karimov, Jamshid H.; Van Wagoner, David R.; Fukamachi, Kiyotaka

    2013-01-01

    Research on the therapeutic modulation of cardiac autonomic tone by electrical stimulation has yielded encouraging early clinical results. Vagus nerve stimulation has reduced the rates of morbidity and sudden death from heart failure, but therapeutic vagus nerve stimulation is limited by side effects of hypotension and bradycardia. Sympathetic nerve stimulation that has been implemented in the experiment may exacerbate the sympathetic-dominated autonomic imbalance. In contrast, concurrent sti...

  6. Cardiac Autonomic Nerve Stimulation in the Treatment of Heart Failure

    OpenAIRE

    Kobayashi, Mariko; Massiello, Alex; Karimov, Jamshid H.; Van Wagoner, David R.; Fukamachi, Kiyotaka

    2013-01-01

    Research on the therapeutic modulation of cardiac autonomic tone by electrical stimulation has yielded encouraging early clinical results. Vagus nerve stimulation has reduced the rates of morbidity and sudden death from heart failure, but therapeutic vagus nerve stimulation is limited by side effects of hypotension and bradycardia. Sympathetic nerve stimulation that has been implemented in the experiment may exacerbate the sympathetic-dominated autonomic imbalance. In contrast, concurrent sti...

  7. Biphasic effects of orexin-A on autonomic nerve activity and lipolysis.

    Science.gov (United States)

    Shen, Jiao; Tanida, Mamoru; Yao, Jia-Fei; Niijima, Akira; Nagai, Katsuya

    2008-10-24

    Previously, we showed that orexin-A, a 33-aa peptide, influences renal sympathetic nerve activity. Because the autonomic nervous system plays an important role in the regulation of lipid metabolism, we investigated the in vivo effects of orexin-A on the sympathetic nerve activity innervating white adipose tissue (WAT-SNA) and lipolysis. We found that intracerebroventricular (icv) administration of orexin-A at doses of 1 microg/rat and 10 ng/rat elevated and suppressed WAT-SNA, respectively. The effect of the high dose of orexin-A (1 microg/rat) was eliminated by pretreatment with diphenhydramine hydrochloride, a histamine H(1) receptor antagonist. In contrast, the effect of the low dose of orexin-A (10 ng/rat) was suppressed by thioperamide maleate salt, a histamine H(3) receptor antagonist. Moreover, icv administration of 1 microg/rat and 10 ng/rat of orexin-A increased and decreased the levels of plasma free fatty acids (FFAs), respectively. The effect of 1 microg/rat of orexin-A on plasma FFA was eliminated by propranolol hydrochloride, a beta-adrenergic receptor blocker, and also by diphenhydramine. The effect of orexin-A at dose of 10 ng/rat disappeared by pretreatment with atropine sulfate, a muscarinic receptor blocker, and thioperamide maleate salt. Our results suggest that high doses of orexin-A may regulate the lipolytic processes in adipose tissue through facilitation of the sympathetic nervous system, which is driven by histamine neurons through the H(1) receptor, and that the beta(3)-receptor may be involved in this enhanced lipolytic response. Low doses of orexin-A, on the other hand, may lower lipolysis by suppressing sympathetic nerve activity via the H(3)-receptor, and the muscarinic receptor may be related to this response.

  8. Neural regulation of the kidney function in rats with cisplatin induced renal failure

    Directory of Open Access Journals (Sweden)

    Niamh E Goulding

    2015-06-01

    Full Text Available Aim: Chronic kidney disease (CKD is often associated with a disturbed cardiovascular homeostasis. This investigation explored the role of the renal innervation in mediating deranged baroreflex control of renal sympathetic nerve activity (RSNA and renal excretory function in cisplatin-induced renal failure.Methods: Rats were either intact or bilaterally renally denervated four days prior to receiving cisplatin (5mg/kg i.p. and entered a chronic metabolic study for 8 days. At day 8, other groups of rats were prepared for acute measurement of RSNA or renal function with either intact or denervated kidneys.Results: Following the cisplatin challenge, creatinine clearance was 50% lower while fractional sodium excretion and renal cortical and medullary TGF-β1 concentrations were 3-4 fold higher in both intact and renally denervated rats compared to control rats. In cisplatin-treated rats, the maximal gain of the high-pressure baroreflex curve was only 20% that of control rats, but not different from that of renally denervated control rats. Volume expansion reduced RSNA by 50% in control and in cisplatin-treated rats but only following bilateral renal denervation. The volume expansion mediated natriuresis/diuresis was absent in the cisplatin-treated rats but was normalised following renal denervation. Conclusions: Cisplatin-induced renal injury impaired renal function and caused a sympatho-excitation with blunting of high and low pressure baroreflex regulation of RSNA, which was dependent on the renal innervation. It is suggested that in man with CKD there is a dysregulation of the neural control of the kidney mediated by its sensory innervation.

  9. Sympathetically evoked Ca2+ signaling in arterial smooth muscle

    Institute of Scientific and Technical Information of China (English)

    Wei-jin ZANG; Joseph ZACHARIA; Christine LAMONT; Withrow Gil WIER

    2006-01-01

    The sympathetic nervous system plays an essential role in the control of total peripheral vascular resistance and blood flow, by controlling the contraction of small arteries. Perivascular sympathetic nerves release ATP, norepinephrine (NE) and neuropeptide Y. This review summarizes our knowledge of the intracellular Ca2+ signals that are activated by ATP and NE, acting respectively on P2X1 and α1 adrenoceptors in arterial smooth muscle. Each neurotransmitter produces a unique type of post-synaptic Ca2+ signal and associated contraction. The neural release of ATP and NE is thought to vary markedly with the pattern of nerve activity, probably reflecting both pre- and post-synaptic mechanisms. Finally, we show that Ca2+ signaling during neurogenic contractions activated by trains of sympathetic nerve fiber action potentials are in fact significantly different from that elicited by simple bath application of exogenous neurotransmitters to isolated arteries (a common experimental technique), and end by identifying important questions remaining in our understanding of sympathetic neurotransmission and the physiological regulation of contraction of small arteries.

  10. 消融肾动脉交感神经对肺动脉高压犬心室收缩功能的影响%Evaluation of the ventricular systolic function in dogs with pulmonary artery hypertension after transcatheter ;renal sympathetic denervation

    Institute of Scientific and Technical Information of China (English)

    胡伟; 赵庆彦; 于胜波; 孙彬; 陈辽; 郭瑞强

    2015-01-01

    目的:应用二维斑点追踪技术评价肾动脉交感神经消融对肺动脉高压犬心脏收缩功能的影响。方法本实验犬分3组:对照组7只,肺高压(PAH)组8只,肾动脉交感神经消融(PAH+RSD)组7只。PAH 组及PAH+RSD组静脉注射脱氢野百合碱,建立肺动脉高压模型,且 PAH+RSD组进一步消融双侧肾动脉交感神经,而对照组及PAH 组做假手术处理。分别于建模前和建模8周后观察比格犬的血压变化及心脏指标变化。测量左室侧壁平均应变、室间隔平均应变、右室侧壁平均应变;通过心尖四腔观左室及右室长轴6个节段二维应变曲线,计算收缩期达峰时间,从而计算左室及右室纵向同步性(LVTsl-6SD、RVTsl-6SD);通过左室心尖水平及二尖瓣水平得到左室扭转曲线,计算左室整体最大扭转角度。结果三组间左室侧壁平均应变无明显变化(P >0.05),PAH+RSD组室间隔平均应变及右室侧壁平均应变明显高于 PAH 组(P <0.01);LVTsl-6SD 和 RVTsl-6SD 在 PAH+RSD 组较 PAH 组明显减低[(25.45±3.59)ms 对(40.40±2.83)ms,P <0.001;(34.16±2.81)ms 对(51.98±3.64)ms,P <0.001];左室整体最大扭转角度在PAH+RSD组明显高于 PAH 组[(10.47±0.73)°对(8.46±1.06)°,P <0.001]。结论肾动脉交感神经消融可以部分抑制肺动脉高压对心室收缩功能的损害作用。%Objective To evaluate the effects of transcatheter renal sympathetic denervation (RSD) on the cardiac systolic function of dogs with pulmonary arterial hypertension(PAH)using two-dimensional speckle tracking imaging (2D-STI).Methods Twenty two dogs were divided in to three groups:control group (n=7),PAH group (n =8),PAH+RSD group(n =7).Pulmonary artery hypertension models were made by monocrotaline injection in PAH group and PAH+RSD group,while bilateral renal artery sympathetic nerve were also ablated in PAH+RSD group.Meanwhile,sham operation treatment were made in the control group and PAH group.The changes

  11. Local denervation of sympathetic nerve from the femoral artery using 6-hydroxydopamine in a rabbit model%6-羟多巴胺去除股动脉交感神经的动物模型建立及相关研究

    Institute of Scientific and Technical Information of China (English)

    靳宇飞; 李富航; 毕龙; 裴国献

    2014-01-01

    目的 探讨6-羟多巴胺(6-OHDA)在体内去除兔股动脉交感神经的可行性,以期为研究单纯血管本身在组织工程骨中有无神经化作用提供理想的动物实验模型. 方法 分离16只新西兰兔右侧股动脉,采用不同药物处理:实验组采用含0.1 mg/mL 6-OHDA和质量百分比为0.1%抗坏血酸Krebs缓冲液处理,为确定药物干预后交感神经的恢复时间,将实验组再分为7d、14d和28 d取材组(n=4);对照组(n=4)采用仅含0.1%抗坏血酸Krebs缓冲液处理.分别用苏木精-伊红(HE)染色、乙醛酸激发单胺荧光染色检测股动脉组织变化、交感神经分布情况,并通过Western blot检测酪酸羟化酶(TH)和神经肽Y(NPY)蛋白表达水平的差异. 结果 HE染色结果显示:与对照组相比,3个取材组股动脉组织血管壁结构完整,无明显形态学改变.乙醛酸激发单胺荧光染色结果显示:对照组股动脉可见大量交感神经呈网状和放射状分布;7d和14 d取材组几乎不可见交感神经,28 d取材组有少量交感神经.Western blot检测结果表明:对照组、7d取材组、14d取材组及28 d取材组TH/β-actin比值平均分别为0.70±0.08、0.19±0.08、0.20±0.06、0.33 ±0.06; NPY/β-actin比值平均分别为0.68±0.14、0.14±0.02、0.17±0.02、0.53±0.10,各取材组的TH和NPY蛋白表达量较对照组均显著减少,而28 d取材组的TH和NPY蛋白表达量较7d、14d取材组明显增多,差异均有统计学意义(P<0.05). 结论 体内局部应用6-OHDA可有效去除股动脉交感神经纤维,是一种可行的血管壁去交感神经方法.本研究建立了一种理想的化学去股动脉交感神经的动物模型.%Objective To explore an effective method to remove sympathetic nerve from the femoral artery in a rabbit model.Methods Femoral arteries from 16 New Zealand rabbits were separated and treated with different drugs.The femoral arteries were processed with Krebs buffer containing 0.1 mg/mL 6

  12. Differential role of nitric oxide in regional sympathetic responses to stimulation of NTS A2a adenosine receptors.

    Science.gov (United States)

    Scislo, Tadeusz J; Tan, Nobusuke; O'Leary, Donal S

    2005-02-01

    Our previous studies showed that preganglionic adrenal (pre-ASNA), renal (RSNA), lumbar, and postganglionic adrenal sympathetic nerve activities (post-ASNA) are inhibited after stimulation of arterial baroreceptors, nucleus of the solitary tract (NTS), and glutamatergic and P2x receptors and are activated after stimulation of adenosine A1 receptors. However, stimulation of adenosine A2a receptors inhibited RSNA and post-ASNA, whereas it activated pre-ASNA. Because the effects evoked by NTS A2a receptors may be mediated via activation of nitric oxide (NO) mechanisms in NTS neurons, we tested the hypothesis that NO synthase (NOS) inhibitors would attenuate regional sympathetic responses to NTS A2a receptor stimulation, whereas NO donors would evoke contrasting responses from pre-ASNA versus RSNA and post-ASNA. Therefore, in chloralose/urethane-anesthetized rats, we compared hemodynamic and regional sympathetic responses to microinjections of selective A2a receptor agonist (CGS-21680, 20 pmol/50 nl) after pretreatment with NOS inhibitors Nomega-nitro-L-arginine methyl ester (10 nmol/100 nl) and 1-[2-(trifluoromethyl)phenyl]imidazole (100 pmol/100 nl) versus pretreatment with vehicle (100 nl). In addition, responses to microinjections into the NTS of different NO donors [40 and 400 pmol/50 nl sodium nitroprusside (SNP); 0.5 and 5 nmol/50 nl 3,3-bis(aminoethyl)-1-hydroxy-2-oxo-1-triazene (DETA NONOate, also known as NOC-18), and 2 nmol/50 nl 3-(2-hydroxy-2-nitroso-1-propylhydrazino)-1-propanamine (PAPA NONOate, also known as NOC-15)], the NO precursor L-arginine (10-50 nmol/50 nl), and sodium glutamate (500 pmol/50 nl) were evaluated. SNP, DETA NONOate, and PAPA NONOate activated pre-ASNA and inhibited RSNA and post-ASNA, whereas l-arginine and glutamate microinjected into the same site of the NTS inhibited all these sympathetic outputs. Decreases in heart rate and depressor or biphasic responses accompanied the neural responses. Pretreatment with NOS inhibitors

  13. Remodelling sympathetic innervation in rat pancreatic islets ontogeny

    Directory of Open Access Journals (Sweden)

    Hiriart Marcia

    2009-06-01

    Full Text Available Abstract Background Pancreatic islets are not fully developed at birth and it is not clear how they are vascularised and innervated. Nerve Growth Factor (NGF is required to guide sympathetic neurons that innervate peripheral organs and also in cardiovascular system and ovary angiogenesis. Pancreatic beta cells of a transgenic mouse that over-expressed NGF in attracts sympathetic hyper-innervation towards them. Moreover, we have previously demonstrated that adult beta cells synthesize and secrete NGF; however, we do not know how is NGF secreted during development, nor if it might be trophic for sympathetic innervation and survival in the pancreas. We analyzed sympathetic innervation and vasculature development in rat pancreatic islets at different developmental stages; foetal (F19, early postnatal (P1, weaning period (P20 and adults. We temporarily correlated these events to NGF secretion by islet cells. Results Sympathetic fibres reached pancreatic islets in the early postnatal period, apparently following blood vessels. The maximal number of sympathetic fibres (TH immunopositive in the periphery of the islets was observed at P20, and then fibres entered the islets and reached the core where beta cells are mainly located. The number of fibres decreased from that stage to adulthood. At all stages studied, islet cells secreted NGF and also expressed the high affinity receptor TrkA. Foetal and neonatal isolated islet cells secreted more NGF than adults. TrkA receptors were expressed at all stages in pancreatic sympathetic fibres and blood vessels. These last structures were NGF–immunoreactive only at early stages (foetal and P0. Conclusion The results suggest that NGF signalling play an important role in the guidance of blood vessels and sympathetic fibres toward the islets during foetal and neonatal stages and could also preserve innervation at later stages of life.

  14. 阿片受体、迷走神经和交感神经在瑞芬太尼诱发兔心血管抑制中的作用%The role of opioid receptors and vagus and sympathetic nerves in remifentanil-induced cardiovascular depression in rabbits

    Institute of Scientific and Technical Information of China (English)

    文益云; 徐军美; 戴如平; 陈恭

    2010-01-01

    Objective To investigate the role of opioid receptors and vagus and sympathetic nerves in the remifentanil-induced cardiovascular depression in rabbits. Methods Forty 2-6 months old New Zealand white rebbits of both sexes weighing 1.5-2.5 kg were randomly divided into 5 groups (n = 8 each): group Ⅰ remifentanil (group R); group Ⅱ naloxone + remifentanil (group N+ R); group Ⅲ vagus nerve cut-off +remifentanil (group V+ R); group Ⅳ epidural block + remifentanil (group S+ R) and group V vagus nerve cutoff + epidural block + remifentanil (group V + S + R). The animals were anesthetized, tracheostomized and mechanically ventilated. PaCO2 was maintained at 35-45 mm Hg. Vecuronium 0.3 mg/kg was given iv every 40 min to keep muscle relaxed. Right carotid artery was cannulated for continuous MAP monitoring. ECG was continuously monitored. A bolus of remifentanil 5.0 μg/kg was administered iv in all 5 groups. In group N + R naloxone 40μg was given iv about 2 min before remifentanil. In group V + R bilateral vagus nerves were cut off through neck incision. After HR and MAP had stabilized for 30 min, remifentanil was given iv. In group S + R epidural block was performed at L6.7 interspace with 2% lidocaine to block cardiac sympathetic nerves. When HR and MAP decreased by 20% of the baseline values and stabilized for 30 min remifentanil was given iv. In group V + S + R bilateral vagus nerves were cut off first. Then epidural block was performed before remifentanil administration. MAP and HR were recorded at 1 min before iv remifentanil administration (T0 ), at 30 s (T1), 1,2, 3, 4, 5, 10, 15 and 20 min (T2-9 ) after remifentanil administration. Results Intravenous remifentanil 5.0 μg/kg significantly decreased HR at T1 and MAP at T1-7 as compared with those at T0 in group R. Pretreatmentwith naloxone 40 μg prevented remifentanil-induced decrease in MAP but did not affect remifentanil-induced decrease in HR in group N + R. Vagus nerve cut-off and sympathetic block

  15. Distinct localization and target specificity of galanin-immunoreactive sympathetic preganglionic neurons of a teleost, the filefish Stephanolepis cirrhifer.

    Science.gov (United States)

    Funakoshi, K; Kadota, T; Atobe, Y; Nakano, M; Hibiya, K; Goris, R C; Kishida, R

    2000-03-15

    Immunoreactivity for galanin was examined in the sympathetic preganglionic neurons in the spinal cord, adrenal glands, sympathetic ganglia, and some sensory ganglia of the filefish Stephanolepis cirrhifer. Galanin-immunoreactive neurons were found only in the rostral part, but not in the caudal part of the central autonomic nucleus (a column of sympathetic preganglionic neurons of teleosts). Many galanin-immunoreactive nerve terminals were found in contact with neurons in the celiac ganglia and the cranial sympathetic ganglia on both sides of the body. Most neurons encircled by galanin-immunoreactive nerve fibers were negative for tyrosine hydroxylase. Galanin-immunoreactive nerve fibers were very sparse in the spinal sympathetic paravertebral ganglia. No galanin-immunoreactive nerve fibers were found in the adrenal glands. No sensory neurons of the trigeminal, vagal, or spinal dorsal root ganglia were positive for galanin-immunoreactivity. These results suggest that galanin-immunoreactive sympathetic preganglionic neurons have distinct segmental localization and might project specifically to a population of non-adrenergic sympathetic postganglionic neurons in the celiac and cranial sympathetic ganglia.

  16. Activation of histamine H3 receptors in human nasal mucosa inhibits sympathetic vasoconstriction.

    Science.gov (United States)

    Varty, LoriAnn M; Gustafson, Eric; Laverty, Maureen; Hey, John A

    2004-01-19

    The peripheral histamine H3 receptor is a presynaptic heterologous receptor located on postganglionic sympathetic nerve fibers innervating sympathetic effector systems such as blood vessels and the heart. An extensive body of evidence shows that activation of the histamine H3 receptor attenuates sympathetic tone by presynaptic inhibition of noradrenaline release. It is proposed that this sympathoinhibitory action, in vivo, leads to reduced vasoconstriction, thereby eliciting a vasodilatory effect. In humans, the peripheral histamine H3 receptor has also been shown to exert a sympathoinhibitory function on specific peripheral autonomic effector systems. For example, human saphenous vein and heart possess functional presynaptic histamine H3 receptors on the sympathetic nerve terminals that upon activation decrease the sympathetic tone to these respective organs. The present studies were conducted to define the role of histamine H3 receptors on neurogenic sympathetic vasoconstrictor responses in human nasal turbinate mucosa. Contractility studies were conducted to evaluate the effect of histamine H3 receptor activation on sympathetic vasoconstriction in surgically isolated human nasal turbinate mucosa. We found that the histamine H3 receptor agonist, (R)-alpha-methylhistamine (30 and 300 nM), inhibited electrical field stimulation-induced (neurogenic) sympathetic vasoconstriction in a concentration-dependent fashion. Pretreatment with the selective histamine H3 receptor antagonist, clobenpropit (100 nM), blocked the sympathoinhibitory effect of (R)-alpha-methylhistamine on the neurogenic sympathetic vasoconstriction. In addition, analysis of Taqman mRNA expression studies showed a specific, high level of distribution of the histamine H3 receptor localized in the human nasal mucosa. Taken together, these studies indicate that histamine H3 receptors modulate vascular contractile responses in human nasal mucosa most likely by inhibiting noradrenaline release from

  17. 肾神经在肾缺血预处理对麻醉家兔心脏保护中的作用%Role of renal nerve in cardioprotection provided by renal ischemic preconditioning in anesthetized rabbits

    Institute of Scientific and Technical Information of China (English)

    丁延峰; 张蔓蔓; 何瑞荣

    2001-01-01

    The effects of renal ischemic preconditioning (RIP) on ischemia-reperfused myocardium were examined in the urethane-anesthetized rabbit to determine whether RIP may provide cardioprotection and to observe the role of the renal nerve in such condition. The results obtained are as follows: (1) During 45 min myocardial ischemia and subsequent 180 min reperfusion, blood pressure, heart rate and myocardial oxygen consumption decreased progressively. Epicardial electrographic ST-segment was elevated significantly in the period of ischemia and returned to the baseline gradually in the course of reperfusion. The myocardial infarct size occupied 55.80±1.25% of the area at risk. (2) RIP significantly reduced the myocardial infarct size to 36.51±2.80% (P<0.01), indicating the cardioprotective effect of such an intervention. (3) Renal nerve section (RNS) completely abolished the cardioprotection afforded by RIP, though RNS per se did not affect the myocardial infarct size produced by ischemia-reperfusion. (4) During 10 min renal ischemia, the averaged multi-unit discharge rate of the renal afferent was increased from 0.14±0.08 to 0.65±0.12 imp/s (P<0.01). (5) Pretreatment with an adenosine receptor antagonist 8-phenyltheophylline (10 mg/kg) markedly attenuated the discharge rate of the renal afferent induced by transient renal ischemia, implying that adenosine released in ischemic kidney activated the renal afferent. It is suggested that activation of renal afferents by transient renal ischemia-reperfusion plays an important role in the cardioprotection afforded by RIP.%在氨基甲酸乙酯麻醉家兔上, 观察肾脏缺血预处理(RIP)对缺血-再灌注心肌的影响, 旨在证实RIP对心肌有无保护效应, 并明确肾神经在其中的作用。所得结果如下: (1)在心脏45 min缺血和180 min再灌注过程中, 血压、心率和心肌耗氧量呈进行性下降;心外膜电图ST段在缺血期明显抬高, 再灌注过程中逐渐恢复到基础对照

  18. Stroke Volume and Sympathetic Responses to Lower-Body Negative Pressure Reveal New Insight into Circulatory Shock in Humans

    Science.gov (United States)

    2004-01-01

    of SBP and twice DBP by three. 2.4. Measurement of stroke volume Stroke volume was measured noninvasively using tho- racic electrical bioimpedance ...received in revised form 25 February 2004; accepted 26 February 2004 Abstract We measured various hemodynamic responses and muscle sympathetic nerve...responses to central hypovolemia. We measured heart rates, arterial blood pressures, sympathetic neural activity (MSNA; peroneal nerve microneurography), and

  19. Incomplete Horner syndrome: Report of a case and description of the sympathetic nervous system anatomy involved in Horner syndrome.

    Science.gov (United States)

    Garbo, Grant M; Harmatz, Alexander J; Isaacson, Glenn

    2011-02-01

    Horner syndrome, in which ptosis, miosis, and anhidrosis occur concomitantly, can arise from injury to the sympathetic nerve pathways anywhere from the brain to the end organs. Incomplete Horner syndrome lacks the sign of anhidrosis. We present a case of incomplete Horner syndrome caused by internal carotid artery dissection and provide a road map of the cervical sympathetic nerves involved in Horner syndrome to explain its etiology. We also discuss the imaging of and therapy for internal carotid artery dissections.

  20. Quantification of sympathetic hyperinnervation and denervation after myocardial infarction by three-dimensional assessment of the cardiac sympathetic network in cleared transparent murine hearts.

    Science.gov (United States)

    Yokoyama, Teruki; Lee, Jong-Kook; Miwa, Keiko; Opthof, Tobias; Tomoyama, Satoki; Nakanishi, Hiroyuki; Yoshida, Akira; Yasui, Haruyo; Iida, Tadatsune; Miyagawa, Shigeru; Okabe, Shigeo; Sawa, Yoshiki; Sakata, Yasushi; Komuro, Issei

    2017-01-01

    The sympathetic nervous system is critical in maintaining the normal physiological function of the heart. Its dysfunction in pathological states may exacerbate the substrate for arrhythmias. Obviously, knowledge of its three-dimensional (3D) structure is important, however, it has been revealed by conventional methods only to a limited extent. In this study, a new method of tissue clearance in combination with immunostaining unravels the 3D structure of the sympathetic cardiac network as well as its changes after myocardial infarction. Hearts isolated from adult male mice were optically cleared using the CUBIC-perfusion protocol. After making the hearts transparent, sympathetic nerves and coronary vessels were immunofluorescently labeled, and then images were acquired. The spatial distribution of sympathetic nerves was visualized not only along the epicardial surface, but also transmurally. They were distributed over the epicardial surface and penetrated into the myocardium to twist around coronary vessels, but also independent from the coronary vasculature. At 2 weeks after myocardial infarction, we were able to quantify both denervation distal from the site of infarction and nerve sprouting (hyperinnervation) at the ischemic border zone of the hearts in a 3D manner. The nerve density at the ischemic border zone was more than doubled in hearts with myocardial infarction compared to intact mice hearts (3D analyses; n = 5, pmyocardial infarction. Both can be visualized and quantified by a new imaging technique in transparent hearts and thereby become a useful tool in elucidating the role of the sympathetic nervous system in arrhythmias associated with myocardial infarction.

  1. Effects of treatment with metoprolol on myocardial nerve growth factor expression and sympathetic sprouting in rats with acute myocardial infarction%美托洛尔对急性心肌梗死大鼠心肌神经生长因子表达和神经重构的影响

    Institute of Scientific and Technical Information of China (English)

    徐振兴; 李京波; 魏盟; 黄冬; 和亚萍

    2008-01-01

    Objective The aim of this study was to explore the effects of β receptor antagonist metoprolol on myocardial nerve growth factor expression and sympathetic nerve sprouting in rats after acute myocardial infarction(AMI). Methods Myocardial infarction was induced by ligation of the left anterior descending coronary artery in 20 rats,which were randomized to MI control group (MI-C,n = 10) and metoprolol treatment group (MI-B,n = 10). Sham-operated group (S,n = 8) was taken randomly as non-infarction control. After four-week treatment with the drug and placebo, the hearts were removed and examined for nerve fiber density . The nerve growth factor expression was measured using Western blot analysis and reverse transcription polymerase chain reaction (RT-PCR). Results The density of nerve fibers with positive immunostaining for growth associated protein 43 (GAP43) and tyrosine hydroxylase (TH) increased in MI-C group compared with the S group after AMI both in the peri-infarct and remote area (P<0.01). Treatment of AMI rats with metoprolol clearly resulted in reduction in Gap43 and TH(P< 0. 01). The level of NGF in MI-C group was also markedly elevated compared with sham rats(P<0.05). After 4-week therapy,metoprolol reduced the production of NGF in the peri-infarct and remote area(P<0.05). Conclusion Early metoprolol treatment after AMI can improve sympathetic sprouting,which is related to inhibition of NGF expression.%目的 探讨β受体阻滞剂美托洛尔对大鼠急性心肌梗死(AMI)后心肌神经生长因子(NGF)表达和交感神经再生的影响.方法 结扎大鼠左前降支,建立AMI模型,存活者随机分为美托洛尔治疗组(MI-B组,n=10)和梗死对照组(MI-C组,n=10),另设假手术组(S组,n=8).MI-B组给予4周美托洛尔治疗,MI-C组和S组给予同体积生理盐水静脉注射和灌胃,4周后检测梗死周边区和梗死远端心脏神经纤维分布和密度以及心肌NGF基因和蛋白表达的变化.结果 与S组相比,MI

  2. Expressions of cardiac sympathetic norepinephrine transporter and β1-adrenergic receptor decreased in aged rats

    Institute of Scientific and Technical Information of China (English)

    He LI; Xiao-qing MA; Fan YE; Jing ZHANG; Xin ZHOU; Zhi-hong WANG; Yu-ming LI; Guo-yuan ZHANG

    2009-01-01

    Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovas-cular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine (NE) transporter (NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleff and maintains the sensitivity of the β-adrenergic receptor (β-AR). In the present study, we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and leff ventricular myocardium in 2- and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA, NET protein and β1-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%, 26%, and 43%, respectively, in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density.

  3. Sympathetic neuroaxonal dystrophy in the aged rat pineal gland.

    Science.gov (United States)

    Schmidt, Robert E; Dorsey, Denise A; Parvin, Curtis A; Beaudet, Lucie N

    2006-10-01

    Dysfunction of circadian melatonin production by the pineal gland in aged humans and rats is thought to reflect the functional loss of its sympathetic innervation. Our ultrastructural neuropathologic studies of the sympathetic innervation of the pineal gland of aged (24 months old) Fischer-344 and Sprague-Dawley rats showed loss of nerve terminals as well as the development of neuroaxonal dystrophy (NAD), an ultrastructurally distinctive distal axonopathy, far in excess of that in young control rats. Immunolocalization of tyrosine hydroxylase confirmed the age-related loss of normal noradrenergic innervation and development of NAD. NAD was more frequent in aged female rats compared to males and was particularly severe in aged female Sprague-Dawley rats compared to Fischer-344 rats. Pineal NGF content was significantly increased or unchanged in female and male aged Fischer-344 rats, respectively, compared to young controls. The rat pineal is a sensitive experimental model for the quantitative ultrastructural examination of age-related neuropathological changes in nerve terminals of postganglionic noradrenergic sympathetic axons, changes which may reflect similar changes in the diffusely distributed sympathetic innervation of other targeted endorgans.

  4. Global- and renal-specific sympathoinhibition in aldosterone hypertension.

    Science.gov (United States)

    Lohmeier, Thomas E; Liu, Boshen; Hildebrandt, Drew A; Cates, Adam W; Georgakopoulos, Dimitrios; Irwin, Eric D

    2015-06-01

    Recent technology for chronic electric activation of the carotid baroreflex and renal nerve ablation provide global and renal-specific suppression of sympathetic activity, respectively, but the conditions for favorable antihypertensive responses in resistant hypertension are unclear. Because inappropriately high plasma levels of aldosterone are prevalent in these patients, we investigated the effects of baroreflex activation and surgical renal denervation in dogs with hypertension induced by chronic infusion of aldosterone (12 μg/kg per day). Under control conditions, basal values for mean arterial pressure and plasma norepinephrine concentration were 100±3 mm Hg and 134±26 pg/mL, respectively. By day 7 of baroreflex activation, plasma norepinephrine was reduced by ≈40% and arterial pressure by 16±2 mm Hg. All values returned to control levels during the recovery period. Arterial pressure increased to 122±5 mm Hg concomitant with a rise in plasma aldosterone concentration from 4.3±0.4 to 70.0±6.4 ng/dL after 14 days of aldosterone infusion, with no significant effect on plasma norepinephrine. After 7 days of baroreflex activation at control stimulation parameters, the reduction in plasma norepinephrine was similar but the fall in arterial pressure (7±1 mm Hg) was diminished (≈55%) during aldosterone hypertension when compared with control conditions. Despite sustained suppression of sympathetic activity, baroreflex activation did not have central actions to inhibit either the stimulation of vasopressin secretion or drinking induced by increased plasma osmolality during chronic aldosterone infusion. Finally, renal denervation did not attenuate aldosterone hypertension. These findings suggest that aldosterone excess may portend diminished blood pressure lowering to global and especially renal-specific sympathoinhibition during device-based therapy.

  5. AMPUTATION AND REFLEX SYMPATHETIC DYSTROPHY

    NARCIS (Netherlands)

    GEERTZEN, JHB; EISMA, WH

    Reflex sympathetic dystrophy is a chronic pain syndrome characterized by chronic burning pain, restricted range of motion, oedema and vasolability. Patients are difficult to treat and the prognosis is very often poor. This report emphasizes that an amputation in case of a reflex sympathetic

  6. Baroreflex control of sympathetic activity in experimental hypertension

    Directory of Open Access Journals (Sweden)

    M.C.C. Irigoyen

    1998-09-01

    Full Text Available The arterial baroreceptor reflex system is one of the most powerful and rapidly acting mechanisms for controlling arterial pressure. The purpose of the present review is to discuss data relating sympathetic activity to the baroreflex control of arterial pressure in two different experimental models: neurogenic hypertension by sinoaortic denervation (SAD and high-renin hypertension by total aortic ligation between the renal arteries in the rat. SAD depresses baroreflex regulation of renal sympathetic activity in both the acute and chronic phases. However, increased sympathetic activity (100% was found only in the acute phase of sinoaortic denervation. In the chronic phase of SAD average discharge normalized but the pattern of discharges was different from that found in controls. High-renin hypertensive rats showed overactivity of the renin angiotensin system and a great depression of the baroreflexes, comparable to the depression observed in chronic sinoaortic denervated rats. However, there were no differences in the average tonic sympathetic activity or changes in the pattern of discharges in high-renin rats. We suggest that the difference in the pattern of discharges may contribute to the increase in arterial pressure lability observed in chronic sinoaortic denervated rats.

  7. 肾去交感神经对心力衰竭犬心室基质重构的影响%Renal sympathetic denervation suppresses ventricular substrate remodeling in a canine high-rate pacing model

    Institute of Scientific and Technical Information of China (English)

    王晓占; 赵庆彦; 于胜波; 王徐乐; 肖金平; 代子玄; 黄鹤; 唐艳红; 黄从新

    2015-01-01

    目的 探讨肾去交感神经(RSD)对心力衰竭(心衰,HF)犬心室基质重构的影响.方法 19只犬按照随机数字表法随机分为3组:假手术组(n=7),心衰组(n=6)和RSD组(n=6).假手术组植入起搏器不起搏;心衰组植入起搏器后行右室快速起搏3周;RSD组先行双侧肾动脉消融再行右室快速起搏3周,实验前后监测血流动力学变化,采用Masson染色、ELISA和Western印迹等方法检测心室间质纤维化、脑钠肽(BNP)、血管紧张素Ⅱ(AngⅡ)、醛固酮和转化生长因子-β(TGF-β)的变化.结果 心衰组和RSD组犬的左右心室舒张末期内径均明显增大[左室:(27.0±2.4)mm 比(37.0±2.8) mm,P<0.01和(30.0±2.5) mm比(36.0±2.8) mm,P<0.05;右室:(11.0±1.5)mm比(14.0±1.7) mm,P=0.03和(12.0±1.1) mm比(14.0±1.2) mm,P<0.05].与RSD组相比,心衰组犬左室舒张末期压力升高[(25.0±3.7) mmHg比(3.3±1.6) mmHg,P<0.01],且心室肌组织纤维化程度明显升高(左室:24.1%±4.8%比8.5%±1.9%,P<0.01;右室:17.2%±5.2%比11.8%±3.9%,P<0.01).与假手术组和RSD组相比,心衰组犬心室中TGF-β表达明显增加,心室肌组织及血清中BNP,AngⅡ和醛固酮水平明显升高.结论 RSD可抑制长期快速心室起搏引起的心室肌基质重构.%Objective To explore the role of renal sympathetic denervation (RSD) on ventricular substrate remodeling in dogs with pacing-induced heart failure (HF).Methods A total of 19 dogs were randomized into 3 groups of sham-operated control (n =7),right ventricular pacing induction of HF (n =6) and RSD (n =6).After 8-week pacing induction of HF.Hemodynamic variables were monitored at baseline and after HF.Masson's trichrome staining,enzyme-linked immunosorbent assay (ELISA) and Western blot were used to measure ventricular interstitial fibrosis,brain natriuretic peptide (BNP),angiotensin Ⅱ (Ang Ⅱ),aldosterone and transforming growth factor-beta (TGF-β).Results All dogs in HF and HF + RSD groups

  8. Sympathetic Blocks Provided Sustained Pain Relief in a Patient with Refractory Painful Diabetic Neuropathy

    Directory of Open Access Journals (Sweden)

    Jianguo Cheng

    2012-01-01

    Full Text Available The sympathetic nervous system has been implicated in pain associated with painful diabetic neuropathy. However, therapeutic intervention targeted at the sympathetic nervous system has not been established. We thus tested the hypothesis that sympathetic nerve blocks significantly reduce pain in a patient with painful diabetic neuropathy who has failed multiple pharmacological treatments. The diagnosis of small fiber sensory neuropathy was based on clinical presentations and confirmed by skin biopsies. A series of 9 lumbar sympathetic blocks over a 26-month period provided sustained pain relief in his legs. Additional thoracic paravertebral blocks further provided control of the pain in the trunk which can occasionally be seen in severe diabetic neuropathy cases, consequent to extensive involvement of the intercostal nerves. These blocks provided sustained and significant pain relief and improvement of quality of life over a period of more than two years. We thus provided the first clinical evidence supporting the notion that sympathetic nervous system plays a critical role in painful diabetic neuropathy and sympathetic blocks can be an effective management modality of painful diabetic neuropathy. We concluded that the sympathetic nervous system is a valuable therapeutic target of pharmacological and interventional modalities of treatments in painful diabetic neuropathy patients.

  9. Renal denervation for resistant hypertension.

    Science.gov (United States)

    Almeida, Manuel de Sousa; Gonçalves, Pedro de Araújo; Oliveira, Eduardo Infante de; Carvalho, Henrique Cyrne de

    2015-02-01

    There is a marked contrast between the high prevalence of hypertension and the low rates of adequate control. A subset of patients with suboptimal blood pressure control have drug-resistant hypertension, in the pathophysiology of which chronic sympathetic hyperactivation is significantly involved. Sympathetic renal denervation has recently emerged as a device-based treatment for resistant hypertension. In this review, the pathophysiological mechanisms linking the sympathetic nervous system and cardiovascular disease are reviewed, focusing on resistant hypertension and the role of sympathetic renal denervation. An update on experimental and clinical results is provided, along with potential future indications for this device-based technique in other cardiovascular diseases. Copyright © 2014 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.

  10. Effect of Bu Yang Huan Wu Decoction (补阳还五汤) Combined with Lumbar Sympathetic Ganglionec-tomy on Recovery of Sciatic Nerve%补阳还五汤和腰交感神经节切除对大鼠坐骨神经损伤的影响

    Institute of Scientific and Technical Information of China (English)

    刘青龙; 秦振龙; 王绣伯

    2014-01-01

    Objective To investigate the effect of Bu Yang Huan Wu decoction (补阳还五汤) and Lumbar Sympathetic Ganglionectomy (LSG) on recovery of sciatic nerve. Methods Sixty Sprague Dawley rats with left sympathectic ganglion injury were divided into two groups. The rats in control group received LSG only while those in the experimental group also took oral administration and medicine bath of Bu Yang Huan Wu decoction (补阳还五汤) as well as LSG. The skin temperature of their left feet, the sciatic nerve function index (SFI) as well as the sciatic nerve conduction velocity (SNCV) were studied before and after injury. Results The skin tem-perature of their left feet in experiment group was higher than that in control group (P<0.05). The recovery of SFT in experimental group was significantly better than that in control group (P<0.01) at 2,4,6 weeks following the experiment. SNCV in the experimental group was significantly faster than that in control group (P<0.01) af-ter Lumbar Sympathetic Ganglionectomy therapy for 2, 4 ,6 weeks. Conclusion Oral administration and medi-cine bath of BuYangHuanWu decoction and LSG is beneficial for injured peripheral nerve.%目的:探讨补阳还五汤和腰交感神经节切除对大鼠坐骨神经损伤的影响。方法:60只SD大鼠损伤左侧坐骨神经,随机分为2组,对照组钳夹并切除腰交感神经节(LSG),实验组在钳夹并切除腰交感神经节后加用补阳还五汤口服及药浴治疗。观察对照组和实验组大鼠左足皮肤温度、坐骨神经功能指数(SFI)和坐骨神经传导速度(SNCV)的差异。结果:实验开始后1、2周实验组皮肤温度较对照组有明显升高(P<0.01)。实验组的坐骨神经功能指数2、4、6周恢复均快于对照组(P<0.01)。分别测实验组、对照组的坐骨神经传导速度。实验组2、4、6周坐骨神经传导速度恢复快于对照组(P<0.01)。结论:补阳还五汤口服加药浴并切除

  11. Activation of NTS A(1) adenosine receptors inhibits regional sympathetic responses evoked by activation of cardiopulmonary chemoreflex.

    Science.gov (United States)

    Ichinose, Tomoko K; Minic, Zeljka; Li, Cailian; O'Leary, Donal S; Scislo, Tadeusz J

    2012-09-01

    Previously we have shown that adenosine operating via the A(1) receptor subtype may inhibit glutamatergic transmission in the baroreflex arc within the nucleus of the solitary tract (NTS) and differentially increase renal (RSNA), preganglionic adrenal (pre-ASNA), and lumbar (LSNA) sympathetic nerve activity (ASNA>RSNA≥LSNA). Since the cardiopulmonary chemoreflex and the arterial baroreflex are mediated via similar medullary pathways, and glutamate is a primary transmitter in both pathways, it is likely that adenosine operating via A(1) receptors in the NTS may differentially inhibit regional sympathetic responses evoked by activation of cardiopulmonary chemoreceptors. Therefore, in urethane-chloralose-anesthetized rats (n = 37) we compared regional sympathoinhibition evoked by the cardiopulmonary chemoreflex (activated with right atrial injections of serotonin 5HT(3) receptor agonist phenylbiguanide, PBG, 1-8 μg/kg) before and after selective stimulation of NTS A(1) adenosine receptors [microinjections of N(6)-cyclopentyl adenosine (CPA), 0.033-330 pmol/50 nl]. Activation of cardiopulmonary chemoreceptors evoked differential, dose-dependent sympathoinhibition (RSNA>ASNA>LSNA), and decreases in arterial pressure and heart rate. These differential sympathetic responses were uniformly attenuated in dose-dependent manner by microinjections of CPA into the NTS. Volume control (n = 11) and blockade of adenosine receptor subtypes in the NTS via 8-(p-sulfophenyl)theophylline (8-SPT, 1 nmol in 100 nl) (n = 9) did not affect the reflex responses. We conclude that activation of NTS A(1) adenosine receptors uniformly inhibits neural and cardiovascular cardiopulmonary chemoreflex responses. A(1) adenosine receptors have no tonic modulatory effect on this reflex under normal conditions. However, when adenosine is released into the NTS (i.e., during stress or severe hypotension/ischemia), it may serve as negative feedback regulator for depressor and sympathoinhibitory reflexes

  12. 脑内活性氧抑制对醋酸去氧皮质酮-盐型高血压大鼠交感神经活动的影响%Effect of inhibiting brain reactive oxygen species on sympathetic nerve activity in DOCA-salt hypertensive rats

    Institute of Scientific and Technical Information of China (English)

    张琪; 谭颖颖

    2014-01-01

    目的:探讨脑内活性氧是否介导醋酸去氧皮质酮(DOCA)-盐型高血压大鼠的交感神经活动增强效应。方法雄性SD大鼠,行左肾切除术后皮下注射DOCA,并饮用1%氯化钠溶液4周,建立DOCA-盐型高血压模型。轻度麻醉状态下,记录大鼠平均动脉压(MAP)、心率(HR)和肾交感神经活动(RSNA);记录基础值后,静脉注射六烃季胺,观察MAP的变化;侧脑室注射tempol(20μmol/L,10μl)或对照液,观察MAP、HR和RSNA的变化。酶联免疫法(ELISA)分析血浆去甲肾上腺素(NE)水平;化学发光法检测下丘脑超氧阴离子水平和NAD(P)H氧化酶活性。结果 DOCA-盐型大鼠的MAP和血浆NE水平较对照组均显著增加(P<0.01);静脉注射神经节阻滞剂六烃季胺,在DOCA-盐型大鼠引起的血压降低是对照大鼠的240%;DOCA-盐型大鼠的下丘脑超氧阴离子水平和NAD(P)H氧化酶活性显著增加(P<0.01);侧脑室微注射tempol在DOCA-盐型大鼠的MAP、HR和RSNA降低与对照组存在显著差异(P<0.01)。结论 DOCA-盐型高血压大鼠可能通过增加下丘脑内NAD(P)H氧化酶来源的活性氧水平,提高交感神经活性,参与高血压的形成和进展。%Objective To investigate whether brain reactive oxygen species mediate sympathoexcitation and arterial pressure elevation in DOCA-salt hypertensive rats. Methods DOCA-salt hypertensive model was established in male SD rats by subcutaneous injection of DOCA after uninephrectomy and drinking 1%NaCl solution for 4 weeks. The baseline mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded in the rats under mild anesthesia, and MAP changes following intravenous hexamethonium injection were observed. The responses of MAP, HR and RSNA to intracerebroventricular administration of tempol (20 μmol/L in 10 μl) were evaluated; plasma NE level was measured with ELISA, and ROS

  13. Relationship between genetic expression of BDNF and NRG-1 and myelinated nerve fiber density and cross-sectional area in thoracic sympathetic trunk of palmar hyperhidrosis%手汗症患者胸交感神经干脑源性神经营养因子和神经调节因子-1基因表达与有髓神经纤维密度及横截面积的关系

    Institute of Scientific and Technical Information of China (English)

    罗荣刚; 涂远荣; 李旭; 林敏; 陈剑锋; 邱明链

    2009-01-01

    Objective To investigate the gene expression of brain-derived neurotrophic factor ( BD-NF) and neuregulin-1 (NRG-1) in thoracic sympathetic trunk and their relation to myelinated nerve fiber density and single myelinated nerve fibers cross-sectional area in palmar hyperhidrosis. Methods Fast red-fast green myelin sheath staining was used to show myelinated nerve fibers. Using the micro-image analysis system,30 cases of myelinated nerve fiber density and single myelinated nerve fibers cross-sectional area were observed in T3 thoracic sympathetic trunk of patients with palmar hyperhidrosis. BDNF and NRG-1 gene expression was also analyzed by RT-PCR. Eight cases of non-palmar hyperhidrosis patients served as controls. Results In 33 thoracic sympathetic trunk of patients with palmar hyperhidrosis, myelinated nerve fiber density and single myelinated nerve fibers cross-sectional area were significantly increased as compared with controls (t = 7. 023,P < 0.05 ; t = 7.462, P < 0.05 respectively). The expression of BDNF and NRG-1 in 33 thoracic sympathetic trunk of patients with palmar hyperhidrosis was 1. 176 00 ± 0.028 70,1. 216 10± 0.075 39 respectively, and that in control group was 1. 037 50 ± 0.053 79,1. 042 70 ± 0.043 57 respectively. The former was significantly higher than the latter ( t = 9.940,P < 0.05 ; t = 6. 195. P < 0.05 respectively). Conclusion BDNF and NRG-I gene over expression increased myelinated nerve fiber density and single myelinated nerve fibers cross-sectional area of thoracic sympathetic trunk in patients with palmar hyperhidro-sis. Thus transmission speed and ability of excitatory of thoracic sympathetic nerve were also increased, which may play a role in the pathogenesis of palmar hyperhidrosis.%目的 观察手汗症患者胸交感神经干脑源性神经营养因子(BDNF)和神经调节因子-1(NRG-1)基因表达及对有髓神经纤维密度和单个纤维横截面积的影响,探讨与手汗症发病机制的关系.方法 采用核

  14. Intermedin in the paraventricular nucleus attenuates cardiac sympathetic afferent reflex in chronic heart failure rats.

    Directory of Open Access Journals (Sweden)

    Xian-Bing Gan

    Full Text Available BACKGROUND AND AIM: Intermedin (IMD is a member of calcitonin/calcitonin gene-related peptide (CGRP family together with adrenomedullin (AM and amylin. It has a wide distribution in the central nervous system (CNS especially in hypothalamic paraventricular nucleus (PVN. Cardiac sympathetic afferent reflex (CSAR is enhanced in chronic heart failure (CHF rats. The aim of this study is to determine the effect of IMD in the PVN on CSAR and its related mechanisms in CHF rats. METHODOLOGY/PRINCIPAL FINDINGS: Rats were subjected to left descending coronary artery ligation to induce CHF or sham-operation (Sham. Renal sympathetic nerve activity (RSNA, mean arterial pressure (MAP and heart rate (HR were recorded. CSAR was evaluated by the RSNA and MAP responses to epicardial application of capsaicin. Acute experiments were carried out 8 weeks after coronary ligation or sham surgery under anesthesia. IMD and angiotensin II (Ang II levels in the PVN were up-regulated in CHF rats. Bilateral PVN microinjection of IMD caused greater decreases in CSAR and the baseline RSNA and MAP in CHF rats than those in Sham rats. The decrease of CSAR caused by IMD was prevented by pretreatment with AM receptor antagonist AM22-52, but not CGRP receptor antagonist CGRP8-37. Ang II in the PVN significantly enhanced CSAR and superoxide anions level, which was inhibited by PVN pretreatment with IMD or tempol (a superoxide anions scavenger in Sham and CHF rats. CONCLUSION: IMD in the PVN inhibits CSAR via AM receptor, and attenuates the effects of Ang II on CSAR and superoxide anions level in CHF rats. PVN superoxide anions involve in the effect of IMD on attenuating Ang II-induced CSAR response.

  15. Relevance of Sympathetic Nervous System Activation in Obesity and Metabolic Syndrome.

    Science.gov (United States)

    Thorp, Alicia A; Schlaich, Markus P

    2015-01-01

    Sympathetic tone is well recognised as being implicit in cardiovascular control. It is less readily acknowledged that activation of the sympathetic nervous system is integral in energy homeostasis and can exert profound metabolic effects. Accumulating data from animal and human studies suggest that central sympathetic overactivity plays a pivotal role in the aetiology and complications of several metabolic conditions that can cluster to form the Metabolic Syndrome (MetS). Given the known augmented risk for type 2 diabetes, cardiovascular disease, and premature mortality associated with the MetS understanding the complex pathways underlying the metabolic derangements involved has become a priority. Many factors have been proposed to contribute to increased sympathetic nerve activity in metabolic abnormalities including obesity, impaired baroreflex sensitivity, hyperinsulinemia, and elevated adipokine levels. Furthermore there is mounting evidence to suggest that chronic sympathetic overactivity can potentiate two of the key metabolic alterations of the MetS, central obesity and insulin resistance. This review will discuss the regulatory role of the sympathetic nervous system in metabolic control and the proposed pathophysiology linking sympathetic overactivity to metabolic abnormalities. Pharmacological and device-based approaches that target central sympathetic drive will also be discussed as possible therapeutic options to improve metabolic control in at-risk patient cohorts.

  16. Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight

    Science.gov (United States)

    Levine, Benjamin D.; Pawelczyk, James A.; Ertl, Andrew C.; Cox, James F.; Zuckerman, Julie H.; Diedrich, Andre; Biaggioni, Italo; Ray, Chester A.; Smith, Michael L.; Iwase, Satoshi; Saito, Mitsuru; Sugiyama, Yoshiki; Mano, Tadaaki; Zhang, Rong; Iwasaki, Kenichi; Lane, Lynda D.; Buckey, Jay C Jr; Cooke, William H.; Baisch, Friedhelm J.; Eckberg, Dwain L.; Blomqvist, C. Gunnar

    2002-01-01

    Orthostatic intolerance is common when astronauts return to Earth: after brief spaceflight, up to two-thirds are unable to remain standing for 10 min. Previous research suggests that susceptible individuals are unable to increase their systemic vascular resistance and plasma noradrenaline concentrations above pre-flight upright levels. In this study, we tested the hypothesis that adaptation to the microgravity of space impairs sympathetic neural responses to upright posture on Earth. We studied six astronauts approximately 72 and 23 days before and on landing day after the 16 day Neurolab space shuttle mission. We measured heart rate, arterial pressure and cardiac output, and calculated stroke volume and total peripheral resistance, during supine rest and 10 min of 60 deg upright tilt. Muscle sympathetic nerve activity was recorded in five subjects, as a direct measure of sympathetic nervous system responses. As in previous studies, mean (+/- S.E.M.) stroke volume was lower (46 +/- 5 vs. 76 +/- 3 ml, P = 0.017) and heart rate was higher (93 +/- 1 vs. 74 +/- 4 beats min(-1), P = 0.002) during tilt after spaceflight than before spaceflight. Total peripheral resistance during tilt post flight was higher in some, but not all astronauts (1674 +/- 256 vs. 1372 +/- 62 dynes s cm(-5), P = 0.32). No crew member exhibited orthostatic hypotension or presyncopal symptoms during the 10 min of postflight tilting. Muscle sympathetic nerve activity was higher post flight in all subjects, in supine (27 +/- 4 vs. 17 +/- 2 bursts min(-1), P = 0.04) and tilted (46 +/- 4 vs. 38 +/- 3 bursts min(-1), P = 0.01) positions. A strong (r(2) = 0.91-1.00) linear correlation between left ventricular stroke volume and muscle sympathetic nerve activity suggested that sympathetic responses were appropriate for the haemodynamic challenge of upright tilt and were unaffected by spaceflight. We conclude that after 16 days of spaceflight, muscle sympathetic nerve responses to upright tilt are normal.

  17. Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system.

    Science.gov (United States)

    Molkov, Yaroslav I; Zoccal, Daniel B; Baekey, David M; Abdala, Ana P L; Machado, Benedito H; Dick, Thomas E; Paton, Julian F R; Rybak, Ilya A

    2014-01-01

    Respiratory modulation seen in the sympathetic nerve activity (SNA) implies that the respiratory and sympathetic networks interact. During hypertension elicited by chronic intermittent hypoxia (CIH), the SNA displays an enhanced respiratory modulation reflecting strengthened interactions between the networks. In this chapter, we review a series of experimental and modeling studies that help elucidate possible mechanisms of sympatho-respiratory coupling. We conclude that this coupling significantly contributes to both the sympathetic baroreflex and the augmented sympathetic activity after exposure to CIH. This conclusion is based on the following findings. (1) Baroreceptor activation results in perturbation of the respiratory pattern via transient activation of postinspiratory neurons in the Bötzinger complex (BötC). The same BötC neurons are involved in the respiratory modulation of SNA, and hence provide an additional pathway for the sympathetic baroreflex. (2) Under hypercapnia, phasic activation of abdominal motor nerves (AbN) is accompanied by synchronous discharges in SNA due to the common source of this rhythmic activity in the retrotrapezoid nucleus (RTN). CIH conditioning increases the CO2 sensitivity of central chemoreceptors in the RTN which results in the emergence of AbN and SNA discharges under normocapnic conditions similar to those observed during hypercapnia in naïve animals. Thus, respiratory-sympathetic interactions play an important role in defining sympathetic output and significantly contribute to the sympathetic activity and hypertension under certain physiological or pathophysiological conditions, and the theoretical framework presented may be instrumental in understanding of malfunctioning control of sympathetic activity in a variety of disease states.

  18. Roles of renal proximal tubule transport in the pathogenesis of hypertension.

    Science.gov (United States)

    Horita, Shoko; Seki, George; Yamada, Hideomi; Suzuki, Masashi; Koike, Kazuhiko; Fujita, Toshiro

    2013-05-01

    Hypertension is a key factor of cardiovascular disease. Many organs and systems including heart, blood vessel, kidney, sympathetic nerve, and endocrine systems are involved in the regulation of blood pressure. In particular, the kidney plays an essential role in the regulation of blood pressure, but is also quite vulnerable to hypertensive tissue damage. For example, most chronic kidney disease (CKD) patients have hypertension and are revealed to have higher mortality than normal population. Furthermore, hypertensive renal sclerosis is emerging as the third main cause of dialysis patients. This mini review is to summarize the effects of angiotensin II and dopamine on renal proximal tubule transport, which may have important roles in the regulation of blood pressure.

  19. Recent advances in sympathetic ophthalmia.

    Science.gov (United States)

    Marak, G E

    1979-01-01

    Recent advances in understanding the pathogenesis of sympathetic ophthalmia are helping to remove the pigmented cloud which has obstructed the view of researchers on this disease for many years. Clinical features, diagnostic testing, histopathologic variations and principles of treatment are evaluated in the context of our increasing understanding of the pathogenesis of this disease. The relationship of sympathetic ophthalmia to Harada's disease and phacoantigenic uveitis are reviewed.

  20. Agmatine suppresses peripheral sympathetic tone by inhibiting N-type Ca(2+) channel activity via imidazoline I2 receptor activation.

    Science.gov (United States)

    Kim, Young-Hwan; Jeong, Ji-Hyun; Ahn, Duck-Sun; Chung, Seungsoo

    2016-08-26

    Agmatine, a putative endogenous ligand of imidazoline receptors, suppresses cardiovascular function by inhibiting peripheral sympathetic tone. However, the molecular identity of imidazoline receptor subtypes and its cellular mechanism underlying the agmatine-induced sympathetic suppression remains unknown. Meanwhile, N-type Ca(2+) channels are important for the regulation of NA release in the peripheral sympathetic nervous system. Therefore, it is possible that agmatine suppresses NA release in peripheral sympathetic nerve terminals by inhibiting Ca(2+) influx through N-type Ca(2+) channels. We tested this hypothesis by investigating agmatine effect on electrical field stimulation (EFS)-evoked contraction and NA release in endothelium-denuded rat superior mesenteric arterial strips. We also investigated the effect of agmatine on the N-type Ca(2+) current in superior cervical ganglion (SCG) neurons in rats. Our study demonstrates that agmatine suppresses peripheral sympathetic outflow via the imidazoline I2 receptor in rat mesenteric arteries. In addition, the agmatine-induced suppression of peripheral vascular sympathetic tone is mediated by modulating voltage-dependent N-type Ca(2+) channels in sympathetic nerve terminals. These results suggest a potential cellular mechanism for the agmatine-induced suppression of peripheral sympathetic tone. Furthermore, they provide basic and theoretical information regarding the development of new agents to treat hypertension.

  1. Morphologic Changes in Autonomic Nerves in Diabetic Autonomic Neuropathy

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    Heung Yong Jin

    2015-12-01

    Full Text Available Diabetic neuropathy is one of the major complications of diabetes, and it increases morbidity and mortality in patients with both type 1 diabetes mellitus (T1DM and type 2 diabetes mellitus (T2DM. Because the autonomic nervous system, for example, parasympathetic axons, has a diffuse and wide distribution, we do not know the morphological changes that occur in autonomic neural control and their exact mechanisms in diabetic patients with diabetic autonomic neuropathy (DAN. Although the prevalence of sympathetic and parasympathetic neuropathy is similar in T1DM versus T2DM patients, sympathetic nerve function correlates with parasympathetic neuropathy only in T1DM patients. The explanation for these discrepancies might be that parasympathetic nerve function was more severely affected among T2DM patients. As parasympathetic nerve damage seems to be more advanced than sympathetic nerve damage, it might be that parasympathetic neuropathy precedes sympathetic neuropathy in T2DM, which was Ewing's concept. This could be explained by the intrinsic morphologic difference. Therefore, the morphological changes in the sympathetic and parasympathetic nerves of involved organs in T1DM and T2DM patients who have DAN should be evaluated. In this review, evaluation methods for morphological changes in the epidermal nerves of skin, and the intrinsic nerves of the stomach will be discussed.

  2. Sympathetic Overactivity in Chronic Kidney Disease: Consequences and Mechanisms

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    Jasdeep Kaur

    2017-08-01

    Full Text Available The incidence of chronic kidney disease (CKD is increasing worldwide, with more than 26 million people suffering from CKD in the United States alone. More patients with CKD die of cardiovascular complications than progress to dialysis. Over 80% of CKD patients have hypertension, which is associated with increased risk of cardiovascular morbidity and mortality. Another common, perhaps underappreciated, feature of CKD is an overactive sympathetic nervous system. This elevation in sympathetic nerve activity (SNA not only contributes to hypertension but also plays a detrimental role in the progression of CKD independent of any increase in blood pressure. Indeed, high SNA is associated with poor prognosis and increased cardiovascular morbidity and mortality independent of its effect on blood pressure. This brief review will discuss some of the consequences of sympathetic overactivity and highlight some of the potential pathways contributing to chronically elevated SNA in CKD. Mechanisms leading to chronic sympathoexcitation in CKD are complex, multifactorial and to date, not completely understood. Identification of the mechanisms and/or signals leading to sympathetic overactivity in CKD are crucial for development of effective therapeutic targets to reduce the increased cardiovascular risk in this patient group.

  3. Implications of Renal Denervation Therapy in Patients with Sleep Apnea

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    Fernando Jaén-Águila

    2015-01-01

    Full Text Available Obstructive sleep apnea (OSA syndrome is a prevalent condition characterized by repeated episodes of obstruction of the upper airway, leading to intermittent hypoxemia and important endothelial and anatomical dysfunctions that cause cardiovascular and cerebrovascular disease. The finding of the relationship between OSA and hypertension, especially resistant hypertension (RHT, has increased the interest in therapeutic strategies that affect renal sympathetic activity in these patients. The observational studies published until now demonstrated that renal denervation therapy can reduce the severity of OSA syndrome. Renal sympathetic denervation (RDN could be a future therapeutic possibility for conditions other than RHT, such as atrial fibrillation, heart failure, obesity, and OSA syndrome, where renal sympathetic system plays an important physiological role. The aim of this review was to elucidate the implications of renal sympathetic activity in OSA syndrome.

  4. Influence of renal denervation on blood pressure, sodium and water excretion in acute total obstructive apnea in rats

    Directory of Open Access Journals (Sweden)

    J.V.M. Franquini

    2009-02-01

    Full Text Available Obstructive apnea (OA can exert significant effects on renal sympathetic nerve activity (RSNA and hemodynamic parameters. The present study focuses on the modulatory actions of RSNA on OA-induced sodium and water retention. The experiments were performed in renal-denervated rats (D; N = 9, which were compared to sham (S; N = 9 rats. Mean arterial pressure (MAP and heart rate (HR were assessed via an intrafemoral catheter. A catheter was inserted into the bladder for urinary measurements. OA episodes were induced via occlusion of the catheter inserted into the trachea. After an equilibration period, OA was induced for 20 s every 2 min and the changes in urine, MAP, HR and RSNA were recorded. Renal denervation did not alter resting MAP (S: 113 ± 4 vs D: 115 ± 4 mmHg or HR (S: 340 ± 12 vs D: 368 ± 11 bpm. An OA episode resulted in decreased HR and MAP in both groups, but D rats showed exacerbated hypotension and attenuated bradycardia (S: -12 ± 1 mmHg and -16 ± 2 bpm vs D: -16 ± 1 mmHg and 9 ± 2 bpm; P < 0.01. The basal urinary parameters did not change during or after OA in S rats. However, D rats showed significant increases both during and after OA. Renal sympathetic nerve activity in S rats increased (34 ± 9% during apnea episodes. These results indicate that renal denervation induces elevations of sodium content and urine volume and alters bradycardia and hypotension patterns during total OA in unconscious rats.

  5. Egr3 dependent sympathetic target tissue innervation in the absence of neuron death.

    Directory of Open Access Journals (Sweden)

    Lin Li

    Full Text Available Nerve Growth Factor (NGF is a target tissue derived neurotrophin required for normal sympathetic neuron survival and target tissue innervation. NGF signaling regulates gene expression in sympathetic neurons, which in turn mediates critical aspects of neuron survival, axon extension and terminal axon branching during sympathetic nervous system (SNS development. Egr3 is a transcription factor regulated by NGF signaling in sympathetic neurons that is essential for normal SNS development. Germline Egr3-deficient mice have physiologic dysautonomia characterized by apoptotic sympathetic neuron death and abnormal innervation to many target tissues. The extent to which sympathetic innervation abnormalities in the absence of Egr3 is caused by altered innervation or by neuron death during development is unknown. Using Bax-deficient mice to abrogate apoptotic sympathetic neuron death in vivo, we show that Egr3 has an essential role in target tissue innervation in the absence of neuron death. Sympathetic target tissue innervation is abnormal in many target tissues in the absence of neuron death, and like NGF, Egr3 also appears to effect target tissue innervation heterogeneously. In some tissues, such as heart, spleen, bowel, kidney, pineal gland and the eye, Egr3 is essential for normal innervation, whereas in other tissues such as lung, stomach, pancreas and liver, Egr3 appears to have little role in innervation. Moreover, in salivary glands and heart, two tissues where Egr3 has an essential role in sympathetic innervation, NGF and NT-3 are expressed normally in the absence of Egr3 indicating that abnormal target tissue innervation is not due to deregulation of these neurotrophins in target tissues. Taken together, these results clearly demonstrate a role for Egr3 in mediating sympathetic target tissue innervation that is independent of neuron survival or neurotrophin deregulation.

  6. Olfactory ensheathing cell transplantation improves sympathetic skin responses in chronic spinal cord injury

    Institute of Scientific and Technical Information of China (English)

    Zuncheng Zheng; Guifeng Liu; Yuexia Chen; Shugang Wei

    2013-01-01

    Forty-three patients with chronic spinal cord injury for over 6 months were transplanted with bryonic olfactory ensheathing cells, 2-4 × 106, into multiple sites in the injured area under the sur-gical microscope. The sympathetic skin response in patients was measured with an electromyo-graphy/evoked potential instrument 1 day before transplantation and 3-8 weeks after trans-tion. Spinal nerve function of patients was assessed using the American Spinal Injury Association impairment scale. The sympathetic skin response was elicited in 32 cases before olfactory en-sheathing celltransplantation, while it was observed in 34 cases after transplantation. tantly, sympathetic skin response latency decreased significantly and amplitude increased cantly after transplantation. Transplantation of olfactory ensheathing cells also improved American Spinal Injury Association scores for movement, pain and light touch. Our findings indicate that factory ensheathing celltransplantation improves motor, sensory and autonomic nerve functions in patients with chronic spinal cord injury.

  7. Interstitial cells of Cajal mediate excitatory sympathetic neurotransmission in guinea pig prostate.

    Science.gov (United States)

    Wang, Jiang-ping; Ding, Guo-fu; Wang, Qin-zhang

    2013-06-01

    Morphological and functional studies have confirmed that interstitial cells of Cajal (ICCs) are involved in many enteric motor neurotransmission pathways. Recent investigations have demonstrated that human and guinea pig prostate glands possess a distinct cell type with morphological and immunological similarities to ICCs. These prostate ICCs have a close relationship with nerve bundles and smooth muscle cells. Prostate smooth muscle tone is largely induced by stimulation from the sympathetic nervous system, which releases excitatory norepinephrine (NE) to act on the α1-adrenoceptor. We have performed morphological and functional experiments to determine the role of ICCs in sympathetic neurotransmission in the guinea pig prostate based on the hypothesis that prostate ICCs act as mediators of sympathetic neurotransmission. Immunohistochemistry revealed many close points of contact between ICCs and sympathetic nerve bundles and smooth muscle cells. Double-labeled sections revealed that α1-adrenoceptor and the gap junction protein connexin 43 were expressed in prostate ICCs. Surprisingly, prostate ICCs co-expressed tyrosine hydroxylase and dopamine β-hydroxylase, two markers of sympathetic neurons. Functionally, the application of NE evoked a large single inward current in isolated prostate ICCs in a dose-dependent manner. The inward current evoked by NE was mediated via the activation of α1-adrenoceptors, because it was abolished by the non-specific α-adrenoceptor antagonist, phentolamine and the specific α1-adrenoceptor antagonist, prazosin. Thus, ICCs in the guinea pig prostate are target cells for prostate sympathetic nerves and possess the morphological and functional characteristics required to mediate sympathetic signals.

  8. Renal Denervation:How Far Have We Got?%肾去神经治疗:How far have we got?

    Institute of Scientific and Technical Information of China (English)

    张杨春

    2012-01-01

    原发性高血压、胰岛素抵抗、充血性心力衰竭、慢性肾功能不全都存在中枢交感神经的过度激活,这种效应来源之一是由肾交感传入神经对中枢交感神经的激活.因此,识别肾交感神经对治疗以上疾病有着重要意义.交感神经系统的长期过度激活还与代谢综合征(如血压的升高、肥胖、血脂代谢紊乱、伴有高胰岛素血症的空腹血糖受损)相关.在此综述中,将说明选择性去除肾交感神经治疗难治性高血压不仅可以降低中枢交感神经的激活,还可影响一些有中枢交感神经过度激活的疾病,如胰岛素抵抗、充血性心力衰竭、利尿剂抵抗和心肾综合征等.%Primary hypertension,insulin resistance,congestive heart failure,and chronic functional renal diseases are all characterized by excessive central sympathetic activation. This effect is attributed to the kidney 'a somatic afferent nerves, which is one source of elevated central sympathetic drive. Chronic activation of the sympathetic nervous system has been related with components of the metabolic syndrome, such as btood pressure elevation, obesity,dyslipidemia,and impaired fasting glucose with hyperin-sulinemia. Tliis article describes the selective removal of renal sympathetic nerves in patients with resistant hypertension, which both reduces the action of the central sympathetic drive and impacts diseases linked with excessive central sympathetic activation.

  9. Differential sympathetic activation in muscle and skin neural districts in the metabolic syndrome.

    Science.gov (United States)

    Grassi, Guido; Quarti-Trevano, Fosca; Seravalle, Gino; Dell'Oro, Raffaella; Dubini, Antonella; Mancia, Giuseppe

    2009-10-01

    The present study was designed to determine whether and to what extent the activation of the sympathetic nervous system reported in the metabolic syndrome is generalized to the whole cardiovascular system or if it is rather confined to selected vascular districts. In 16 untreated patients with metabolic syndrome, 12 essential hypertensive subjects, 12 obese subjects, and 14 lean healthy normotensive controls, we measured blood pressure (Finapres, Englewood, CO), heart rate (electrocardiogram), venous plasma norepinephrine (high-performance liquid chromatography), and postganglionic sympathetic nerve traffic in the skeletal muscle and in the skin districts (microneurography). The muscle and skin nerve traffic measurements were obtained in a randomized sequence. Measurements also included skin sympathetic nerve responses to an arousal (acoustic stimulus). The 4 groups of subjects had superimposable ages. Muscle sympathetic nerve traffic values were significantly higher in subjects with hypertension and in those with obesity than in controls (51.2 +/- 2.8 and 52.0 +/- 3.0 vs 37.2 +/- 3.3 bursts per 100 heart beats, respectively; P fashion by the various components of the disease.

  10. A review of facial nerve anatomy.

    Science.gov (United States)

    Myckatyn, Terence M; Mackinnon, Susan E

    2004-02-01

    An intimate knowledge of facial nerve anatomy is critical to avoid its inadvertent injury during rhytidectomy, parotidectomy, maxillofacial fracture reduction, and almost any surgery of the head and neck. Injury to the frontal and marginal mandibular branches of the facial nerve in particular can lead to obvious clinical deficits, and areas where these nerves are particularly susceptible to injury have been designated danger zones by previous authors. Assessment of facial nerve function is not limited to its extratemporal anatomy, however, as many clinical deficits originate within its intratemporal and intracranial components. Similarly, the facial nerve cannot be considered an exclusively motor nerve given its contributions to taste, auricular sensation, sympathetic input to the middle meningeal artery, and parasympathetic innervation to the lacrimal, submandibular, and sublingual glands. The constellation of deficits resulting from facial nerve injury is correlated with its complex anatomy to help establish the level of injury, predict recovery, and guide surgical management.

  11. Maturational changes in sympathetic and sensory innervation of the rat uterus: effects of neonatal capsaicin treatment.

    Science.gov (United States)

    Brauer, M M; Lincoln, J; Sarner, S; Blundell, D; Milner, P; Passaro, M; Burnstock, G

    1994-04-01

    The plasticity of the sympathetic and sensory innervation of the rat uterus was examined, before and after puberty, in controls and in animals where primary sensory nerves had been destroyed by neonatal capsaicin treatment. Immunohistochemical and histochemical methods were used in association with nerve density measurements and biochemical assays. The main findings were as follows: (1) Puberty was associated with a marked increase in the weight of the uterine horn, uterine cervix and parametrial tissue. This was unaffected by capsaicin treatment. (2) The sympathetic innervation of the uterine horn and parametrial tissue was reduced following puberty as revealed by a decrease in the density of noradrenaline-containing nerves and a marked decrease in the tissue concentration of noradrenaline. Sympathetic nerves supplying the uterine cervix and the blood vessels of the uterus appeared to be unaffected by puberty. (3) In contrast, the sensory supply of the uterus by substance P and calcitonin gene-related peptide-containing nerves increased in parallel with uterine growth during puberty resulting in no change in nerve density and only a slight reduction in peptide concentration. (4) Neonatal capsaicin treatment caused a long-lasting depletion of substance P- and calcitonin gene-related peptide-containing nerves. In the uterine horn and parametrial tissue, capsaicin-resistant calcitonin gene-related peptide, but not substance P, still increased with tissue weight during puberty, indeed, in the uterine horn, the relative increase was greater than in controls. (5) Sensory denervation resulted in an increase in the non-vascular sympathetic supply of the uterus, although there was a regional variation in the time course of the response. Perivascular sympathetic nerves were unaffected by capsaicin treatment. The pattern of change in non-vascular noradrenaline-containing nerves associated with puberty was similar in nature to controls. Thus, there is considerable plasticity

  12. Stimulation of NTS A1 adenosine receptors differentially resets baroreflex control of regional sympathetic outputs.

    Science.gov (United States)

    Scislo, Tadeusz J; Ichinose, Tomoko K; O'Leary, Donal S

    2008-01-01

    Previously we showed that pressor and differential regional sympathoexcitatory responses (adrenal > renal >/= lumbar) evoked by stimulation of A(1) adenosine receptors located in the nucleus of the solitary tract (NTS) were attenuated/abolished by baroreceptor denervation or blockade of glutamatergic transmission in the NTS, suggesting A(1) receptor-elicited inhibition of glutamatergic transmission in baroreflex pathways. Therefore we tested the hypothesis that stimulation of NTS A(1) adenosine receptors differentially inhibits/resets baroreflex responses of preganglionic adrenal (pre-ASNA), renal (RSNA), and lumbar (LSNA) sympathetic nerve activity. In urethane-chloralose-anesthetized male Sprague-Dawley rats (n = 65) we compared baroreflex-response curves (iv nitroprusside and phenylephrine) evoked before and after bilateral microinjections into the NTS of A(1) adenosine receptor agonist (N(6)-cyclopentyladenosine, CPA; 0.033-330 pmol/50 nl). CPA evoked typical dose-dependent pressor and differential sympathoexcitatory responses and similarly shifted baroreflex curves for pre-ASNA, RSNA, and LSNA toward higher mean arterial pressure (MAP) in a dose-dependent manner; the maximal shifts were 52.6 +/- 2.8, 48.0 +/- 3.6, and 56.8 +/- 6.7 mmHg for pre-ASNA, RSNA, and LSNA, respectively. These shifts were not a result of simple baroreceptor resetting because they were two to three times greater than respective increases in baseline MAP evoked by CPA. Baroreflex curves for pre-ASNA were additionally shifted upward: the maximal increases of upper and lower plateaus were 41.8 +/- 16.4% and 45.3 +/- 8.7%, respectively. Maximal gain (%/mmHg) measured before vs. after CPA increased for pre-ASNA (3.0 +/- 0.6 vs. 4.9 +/- 1.3), decreased for RSNA (4.1 +/- 0.6 vs. 2.3 +/- 0.3), and remained unaltered for LSNA (2.1 +/- 0.2 vs. 2.0 +/- 0.1). Vehicle control did not alter the baroreflex curves. We conclude that the activation of NTS A(1) adenosine receptors differentially inhibits

  13. Sympathetic nervous activation in obesity and the metabolic syndrome--causes, consequences and therapeutic implications.

    Science.gov (United States)

    Lambert, Gavin W; Straznicky, Nora E; Lambert, Elisabeth A; Dixon, John B; Schlaich, Markus P

    2010-05-01

    The world wide prevalence of obesity and the metabolic syndrome is escalating. Contrary to earlier experimental evidence, human obesity is characterised by sympathetic nervous activation, with the outflows to both the kidney and skeletal muscle being activated. While the mechanisms responsible for initiating the sympathetic activation remain to be unequivocally elucidated, hyperinsulinemia, obstructive sleep apnoea, increased circulating adipokines, stress and beta adrenergic receptor polymorphisms are implicated. The pattern of sympathetic activation may be the pathophysiological mechanism underpinning much obesity-related illnesses with the consequences including, amongst others, the development of hypertension, insulin resistance, diastolic dysfunction and renal impairment. While diet and exercise are the first line therapy for the treatment of obesity and the metabolic syndrome, pharmacological interventions targeting the sympathetic nervous system, either directly or indirectly are also likely to be of benefit. Importantly, the benefit may not necessarily be weight related but may be associated with a reduction in end organ damage.

  14. Effect of inhibition of nitric oxide synthase on blood pressure and renal sodium handling in renal denervated rats

    Directory of Open Access Journals (Sweden)

    F. Xavier

    2000-03-01

    Full Text Available The role of sympathetic nerve activity in the changes in arterial blood pressure and renal function caused by the chronic administration of NG-nitro-L-arginine methyl ester (L-NAME, an inhibitor of nitric oxide (NO synthesis, was examined in sham and bilaterally renal denervated rats. Several studies have demonstrated that sympathetic nerve activity is elevated acutely after L-NAME administration. To evaluate the role of renal nerve activity in L-NAME-induced hypertension, we compared the blood pressure response in four groups (N = 10 each of male Wistar-Hannover rats weighing 200 to 250 g: 1 sham-operated vehicle-treated, 2 sham-operated L-NAME-treated, 3 denervated vehicle-treated, and 4 denervated L-NAME-treated rats. After renal denervation or sham surgery, one control week was followed by three weeks of oral administration of L-NAME by gavage. Arterial pressure was measured weekly in conscious rats by a tail-cuff method and renal function tests were performed in individual metabolic cages 0, 7, 14 and 21 days after the beginning of L-NAME administration. L-NAME (60 mg kg-1 day-1 progressively increased arterial pressure from 108 ± 6.0 to 149 ± 12 mmHg (P<0.05 in the sham-operated group by the third week of treatment which was accompanied by a fall in creatinine clearance from 336 ± 18 to 222 ± 59 µl min-1 100 g body weight-1 (P<0.05 and a rise in fractional urinary sodium excretion from 0.2 ± 0.04 to 1.62 ± 0.35% (P<0.05 and in sodium post-proximal fractional excretion from 0.54 ± 0.09 to 4.7 ± 0.86% (P<0.05. The development of hypertension was significantly delayed and attenuated in denervated L-NAME-treated rats. This was accompanied by a striking additional increase in fractional renal sodium and potassium excretion from 0.2 ± 0.04 to 4.5 ± 1.6% and from 0.1 ± 0.015 to 1.21 ± 0.37%, respectively, and an enhanced post-proximal sodium excretion compared to the sham-operated group. These differences occurred despite an

  15. Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy in humans.

    Science.gov (United States)

    Moak, Jeffrey P; Eldadah, Basil; Holmes, Courtney; Pechnik, Sandra; Goldstein, David S

    2005-06-01

    Upper thoracic sympathectomy is used to treat several disorders. Sympathetic nerve fibers emanating from thoracic ganglia innervate the heart. Whether unilateral or bilateral upper thoracic sympathectomy affects cardiac sympathetic innervation in humans in vivo has been unclear. The purpose of this study was to assess whether thoracic sympathectomy decreases cardiac sympathetic innervation, as indicated by positron emission tomographic scanning after intravenous injection of the sympathoneural imaging agent 6-[18F]fluorodopamine. Nine patients with previous upper thoracic sympathectomies (four right-sided, one left-sided, four bilateral) underwent thoracic 6-[18F]fluorodopamine scanning between 1 and 2 hours after injection of the imaging agent. In each case, a low rate of entry of norepinephrine into the arm venous drainage (norepinephrine spillover) verified upper limb sympathectomy. Data were compared with those from the interventricular septum of patients with cardiac sympathetic denervation associated with pure autonomic failure and from normal volunteers. All four patients with bilateral sympathectomy had low septal myocardial 6-[18F]fluorodopamine-derived radioactivity (2,673 +/- 92 nCi-kg/cc-mCi at an average of 89 minutes after injection) compared with normal volunteers (3,634 +/- 311 nCi-kg/cc-mCi at 83 minutes, N = 22, P = .007) and higher radioactivity than in patients with pure autonomic failure (1,320 +/- 300 nCi-kg/cc-mCi at 83 minutes, N = 7, P = .003). Patients with unilateral sympathectomy had normal 6-[18F]fluorodopamine-derived radioactivity (3,971 +/- 337 nCi-kg/cc-mCi at 87 minutes). Bilateral upper thoracic sympathectomy partly decreases cardiac sympathetic innervation density.

  16. In vivo demonstration of H3-histaminergic inhibition of cardiac sympathetic stimulation by R-α-methyl-histamine and its prodrug BP 2.94 in the dog

    OpenAIRE

    Mazenot, Catherine; Ribuot, Christophe; Durand, Andrée; Joulin, Yves; Demenge, Pierre; Godin-Ribuot, Diane

    1999-01-01

    The aim of this study was to investigate whether histamine H3-receptor agonists could inhibit the effects of cardiac sympathetic nerve stimulation in the dog.Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the right cardiac sympathetic nerves (1–4 Hz, 10 V, 10 ms) in the anaesthetized dog treated with R-α-methyl-histamine (R-HA) and its prodrug BP 2.94 (BP).Cardiac sympathetic stimulation induced a noradr...

  17. The History of Sympathetic Surgery.

    Science.gov (United States)

    Hashmonai, Moshe

    2016-11-01

    At present, primary hyperhidrosis is the main indication for sympathectomy. For upper thoracic sympathetic ablation, excision of the second thoracic ganglion alone or with the first and/or third ganglia was the standard during the open surgery era. With the advent of thoracoscopy, modifications related to the level, extent, and type of ablation were proposed to attenuate compensatory hyperhidrosis. The ideal operation for sympathetic denervation of the face and upper limbs remain to be defined. Controlled double-blind studies with quantitave measurements of sweat production are required. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Joint UK societies’ 2014 consensus statement on renal denervation for resistant hypertension

    Science.gov (United States)

    Lobo, Melvin D; de Belder, Mark A; Cleveland, Trevor; Collier, David; Dasgupta, Indranil; Deanfield, John; Kapil, Vikas; Knight, Charles; Matson, Matthew; Moss, Jonathan; Paton, Julian F R; Poulter, Neil; Simpson, Iain; Williams, Bryan; Caulfield, Mark J

    2015-01-01

    Resistant hypertension continues to pose a major challenge to clinicians worldwide and has serious implications for patients who are at increased risk of cardiovascular morbidity and mortality with this diagnosis. Pharmacological therapy for resistant hypertension follows guidelines-based regimens although there is surprisingly scant evidence for beneficial outcomes using additional drug treatment after three antihypertensives have failed to achieve target blood pressure. Recently there has been considerable interest in the use of endoluminal renal denervation as an interventional technique to achieve renal nerve ablation and lower blood pressure. Although initial clinical trials of renal denervation in patients with resistant hypertension demonstrated encouraging office blood pressure reduction, a large randomised control trial (Symplicity HTN-3) with a sham-control limb, failed to meet its primary efficacy end point. The trial however was subject to a number of flaws which must be taken into consideration in interpreting the final results. Moreover a substantial body of evidence from non-randomised smaller trials does suggest that renal denervation may have an important role in the management of hypertension and other disease states characterised by overactivation of the sympathetic nervous system. The Joint UK Societies does not recommend the use of renal denervation for treatment of resistant hypertension in routine clinical practice but remains committed to supporting research activity in this field. A number of research strategies are identified and much that can be improved upon to ensure better design and conduct of future randomised studies. PMID:25431461

  19. Acute and chronic estrogen supplementation decreases uterine sympathetic innervation in ovariectomized adult virgin rats.

    Science.gov (United States)

    Zoubina, E V; Mize, A L; Alper, R H; Smith, P G

    2001-10-01

    Uterine innervation undergoes substantial reorganization associated with changes in reproductive status. Nerves innervating the uterus are decreased in pregnancy and puberty, and even the normal rodent estrous cycle is characterized by fluctuations in numbers of myometrial nerve fibers. During the follicular (proestrus/estrous) phase of the estrous cycle, intact nerves are rapidly depleted and then return over the next 2-3 days in the luteal (metestrus/diestrus) phase. We hypothesize that uterine nerve depletion is initiated by increased circulating estrogen in the follicular phase. However, studies have not shown whether estrogen can reduce uterine innervation and, if so, whether the time course is compatible with the rapid changes observed in the estrous cycle. These questions were addressed in the present study. Mature ovariectomized virgin rats received 17-beta-estradiol as a single injection (10 microg/kg s.c.) or chronically from timed-release pellets (0.1 microg/pellet for 3 weeks sustained release). Total (protein gene-product 9.5-immunoreactive) and sympathetic (dopamine beta-hydroxylase-immunoreactive) uterine innervation was assessed quantitatively. Both total and sympathetic innervation was abundant in uterine longitudinal smooth muscle of ovariectomized rats. However, following acute or chronic estrogen administration, total and sympathetic fiber numbers were markedly decreased. This was not due to altered uterine size, as reductions persisted after correcting for size differences. Our results indicate that sympathetic nerves are lost from uterine smooth muscle after estradiol treatment in a manner similar to that seen in the intact animal during estrus and pregnancy. This suggests that the rise in estradiol prior to estrus is sufficient to deplete uterine sympathetic innervation.

  20. Sympathetic re-innervation after heart transplantation: dual-isotope neurotransmitter scintigraphy, norepinephrine content and historical examination

    Energy Technology Data Exchange (ETDEWEB)

    Guertner, C. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Nuclear Medicine; Krause, B.J. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Nuclear Medicine; Klepzig, H. Jr. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Cardiology; Herrmann, G. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Pathology; Lelbach, S. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Nuclear Medicine; Vockert, E.K. [Biocenter Niederursel, Frankfurt am Main (Germany). Dept. of Pharmacology; Hartmann, A. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Cardiology; Maul, F.D. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Nuclear Medicine; Kranert, T.W. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Nuclear Medicine; Mutschler, E. [Biocenter Niederursel, Frankfurt am Main (Germany). Dept. of Pharmacology; Huebner, K. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Pathology; Hoer, G. [Univ. Hospital Frankfurt am Main (Germany). Dept. of Nuclear Medicine

    1995-05-01

    Cardiac transplantation entails surgical disruption of the sympathetic nerve fibres from their somata, resulting in sympathetic denervation. In order to investigate the occurrence of sympathetic re-innervation, neurotransmitter scintigraphy using the norepinephrine analogue iodine-123 metaiodobenzylguanidine (MIBG) was performed in 15 patients 2-69 months after transplantation. In addition, norepinephrine content and immunohistochemical reactions of antibodies to Schwann cell-associated S100 protein, to neuron-specific enolase (NSE) and to norepinephrine were examined in 34 endomyocardial biopsies of 29 patients 1-88 months after transplantation. Anterobasal {sup 123}I-MIBG uptake indicating partial sympathetic re-innervation could be shown in 40% of the scintigraphically investigated patients 37-69 months after transplantation. In immunohistochemical studies 83% of the patients investigated 1-72 Months after transplantation showed nerve fibres in their biopsies but not positive reaction to norepinephrine. Significant norepinephrine content indicating re-innervation could not be detected in any biopsy. It was concluded that in spite of the lack of norepinephrine content there seemed to be immunohistological and scintigraphic evidence of sympathetic re-innervation. An explanation for this contradictory finding may be the reduced or missing norepinephrine storage ability compared to the restored uptake ability of regenerated sympathetic nerve fibres. (orig.)

  1. 神经传导检测结合交感皮肤反应及R-R间期变化率对糖尿病周围神经病的诊断价值%Significance of nerve conduction velocity with sympathetic skin response and R-R interval variation in the diagnosis of diabetic peripheral neuropathy

    Institute of Scientific and Technical Information of China (English)

    汪飞; 叶梦鸽; 胡敏; 孙晓霞; 胡琛亮; 吴和; 王建中

    2012-01-01

    To investigate the significance of nerve conduction study(NCS) with sympathetic skin response(SSR) and R-R interval variation( RRIV) in the diagnosis of diabetic peripheral neu-ropathy(DPN). Methods; Eighty-two diabetic patients(DM group) and age-and gender-matched volun-teers(controls) underwent NCS.SSR.RRIV. The DM group was divided into subgroups with or without symptoms according to the clinical sensory motor nerves damages,or divided into subgroups with normal or abnormal NCS. Results: (1)The parameters of SSR and RRIV were significantly related to scores of clinical autonomic nerve dysfunction(all P<0. 05); (2) As compared with the healthy controls,the abnormality rate of NCS increased(P<0. 01),latency of SSR was prolonged and amplitude of SSR decreased, parameters of RRIV decreased in DM group whether with or without symptoms(all P<0. 05) . The abnormality rate of NCS in DM group with symptoms was higher than that in DM group without symptoms (P<0. 01) . Tshere was no significant difference of SSR was and RRIV between the two groups) (3) Compared with the healthy controls, latency of SSR prolonged and amplitude of SSR decreased, parameters of RRIV decreased in DM group with abnormal NCS(P<0. 05) (latency of SSR in upper limbs pro- , longed and amplitude of that decreased(P<05) .while parameters of SSR in lower limbs and RRIV had no significant change in DM group with normal NCS. There was no significant difference of SSR andRRIV between the two DM subgroups. Conclusion: NCS and SSR.RRIV are objective and effective methods to detect sensory and motor nerves and autonomic nerves damages respectively,and to discover sub-clinical lesions. There is no parallel relationship between involvement of sensory motor nerves and that of autonomic nerves in DPNCcombined use of the three methods can give a comprehensive evalution of peripheral neuropathy.%目的:探讨神经传导检测(NCS)结合交感皮肤反应(SSR)及心电图R-R间期变化率(RRIV)对糖尿病周围

  2. Sympathetic hyperinnervation of the uterus in the estrogen receptor alpha knock-out mouse.

    Science.gov (United States)

    Zoubina, E V; Smith, P G

    2001-01-01

    Uterine innervation undergoes cyclical remodeling in the adult virgin rat. Previous studies showed that ovariectomy leads to increased uterine sympathetic nerve density, and this can be reduced by estrogen administration. However, the receptor mechanism by which estrogen modulates sympathetic innervation is unknown. The present study assessed the role of the estrogen receptor alpha in establishing levels of uterine innervation by comparing the nerve abundance in mice with a null mutation of the estrogen receptor alpha with those of the wild-type cycling mouse. Immunostaining for total uterine innervation using antibodies against the pan-neuronal marker protein gene product 9.5 showed that nerve numbers in normally cycling wild-type mice were high in diestrus when circulating estrogen is at its nadir, and low at estrus, coincident with high plasma estrogen. Uteri of the estrogen receptor alpha knock-out mice were smaller than those of wild-type mice, but even when corrected for differences in size, total innervation was 188% and 355% greater than that of wild-type mice at diestrus and estrus, respectively. This hyperinnervation is associated with increased numbers of nerves immunoreactive for the noradrenergic enzyme dopamine beta-hydroxylase, without obvious differences in those containing calcitonin gene-related peptide or the vesicular acetylcholine transporter. While estrogen supplementation of the ovariectomized wild-type mice significantly reduced total uterine innervation, neither ovariectomy nor estrogen supplementation affected uterine nerve density in estrogen receptor alpha knock-out mice.We conclude that estrogen acting through the estrogen receptor alpha determines the number of sympathetic nerve terminal branches within uterine smooth muscle target. In mice with low circulating estrogen, or high estrogen but lacking the functional estrogen receptor alpha, the uterus contains abundant sympathetic nerves, whereas estrogen acts via the estrogen receptor

  3. Central SDF-1/CXCL12 expression and its cardiovascular and sympathetic effects: the role of angiotensin II, TNF-α, and MAP kinase signaling.

    Science.gov (United States)

    Wei, Shun-Guang; Zhang, Zhi-Hua; Yu, Yang; Felder, Robert B

    2014-12-01

    The chemokine stromal cell-derived factor-1 (SDF-1/CXCL12) and its receptors are expressed by neurons and glial cells in cardiovascular autonomic regions of the brain, including the hypothalamic paraventricular nucleus (PVN), and contribute to neurohumoral excitation in rats with ischemia-induced heart failure. The present study examined factors regulating the expression of SDF-1 in the PVN and mechanisms mediating its sympatho-excitatory effects. In urethane anesthetized rats, a 4-h intracerebroventricular (ICV) infusion of angiotensin II (ANG II) or tumor necrosis factor-α (TNF-α) in doses that increase mean blood pressure (MBP) and sympathetic drive increased the expression of SDF-1 in PVN. ICV administration of SDF-1 increased the phosphorylation of p44/42 mitogen-activated protein kinase (MAPK), JNK, and p38 MAPK in PVN, along with MBP, heart rate (HR), and renal sympathetic nerve activity (RSNA), but did not affect total p44/42 MAPK, JNK, and p38 MAPK levels. ICV pretreatment with the selective p44/42 MAPK inhibitor PD98059 prevented the SDF-1-induced increases in MBP, HR, and RSNA; ICV pretreatment with the selective JNK and p38 MAPK inhibitors attenuated but did not block these SDF-1-induced excitatory responses. ICV PD98059 also prevented the sympatho-excitatory response to bilateral PVN microinjections of SDF-1. ICV pretreatment with SDF-1 short-hairpin RNA significantly reduced ANG II- and TNF-α-induced phosphorylation of p44/42 MAPK in PVN. These findings identify TNF-α and ANG II as drivers of SDF-1 expression in PVN and suggest that the full expression of their cardiovascular and sympathetic effects depends upon SDF-1-mediated activation of p44/42 MAPK signaling.

  4. Effect of excision of peripheral sympathetic nerve network in common carotid artery in children with cerebral palsy and its effect on their cognitive function%颈总动脉周围交感神经网剥脱切除术治疗脑性瘫痪患儿的效果及对其认知功能的影响

    Institute of Scientific and Technical Information of China (English)

    赵家鹏; 王家勤; 常崇旺; 王玉峰; 马世江; 冯宇飞

    2015-01-01

    Objective To explore the clinical effect of excision of peripheral sympathetic nerve network in common carotid artery on children with cerebral palsy (CP)and the effect on their cognitive function. Methods A ret-rospective study method was admitted to preschool children with CP in 69 cases in Center of Brain Disease,the Third Hospital Affiliated to Xinxiang Medical University from July 2008 to August 2014, the common carotid artery sympathetic with the surrounding network stripping off resection treatment of 43 cases ( surgery group) ,without the use of surgery in the treatment of children with 26 cases ( no operation group) . The muscle tension improved, movement to improve the ability of 2 groups before and after treatment 6 months were detected and compared. Developmental quotient ( DQ) ,intelligence quotient ( IQ) ,bilateral middle cerebral artery ( MCA) hemodynamic index difference were deter-mined between 2 groups before and after treatment 6 months. Results After treatment 6 months,the muscle tension score and walking ability score of the surgery group were significantly better than those of no operation group [(2. 2± 1. 1) scores vs (4. 5±0. 6)scores,(3. 5±0. 7) scores vs (2. 7±0. 8) scores,all P<0. 05],and significantly improved compared with before treatment[(4. 8±0. 6)scores,(2. 2±0. 9)scores,all P<0. 05]. After treatment 6 months,the IQ score,fine motor, social adaptation, personal social, language score and MCA mean velocity ( MV ) , peak velocity ( PV) ,resistance index ( RI) ,pulsatility index ( PI) determination value of the surgery group were significantly higher than those of no operation group and before treatment (all P<0. 05). Conclusions Excision of peripheral sympathetic nerve network on common carotid artery has a good clinical effect in the treatment of CP , and can significantly improve the cognitive function of children with CP .%目的:探讨颈总动脉周围交感神经网剥脱切除术治疗脑性瘫痪( CP )患儿的临床

  5. Angiotensin-(1-7 relieved renal injury induced by chronic intermittent hypoxia in rats by reducing inflammation, oxidative stress and fibrosis

    Directory of Open Access Journals (Sweden)

    W. Lu

    Full Text Available We aimed to study the renal injury and hypertension induced by chronic intermittent hypoxia (CIH and the protective effects mediated by angiotensin 1-7 [Ang(1-7]. We randomly assigned 32 male Sprague-Dawley rats (body weight 180-200 g to normoxia control, CIH, Ang(1-7-treated normoxia, and Ang(1-7-treated CIH groups. Systolic blood pressure (SBP was monitored at the start and end of each week. Renal sympathetic nerve activity (RSNA was recorded. CTGF and TGF-β were detected by immunohistochemistry and western blotting. Tissue parameters of oxidative stress were also determined. In addition, renal levels of interleukin-6, tumor necrosis factor-α, nitrotyrosine, and hypoxia-inducible factor-1α were determined by immunohistochemistry, immunoblotting, and ELISA. TUNEL assay results and cleaved caspase 3 and 12 were also determined. Ang(1-7 induced a reduction in SBP together with a restoration of RSNA in the rat model of CIH. Ang(1-7 treatment also suppressed the production of reactive oxygen species, reduced renal tissue inflammation, ameliorated mesangial expansion, and decreased renal fibrosis. Thus, Ang(1-7 treatment exerted renoprotective effects on CIH-induced renal injury and was associated with a reduction of oxidative stress, inflammation and fibrosis. Ang(1-7 might therefore represent a promising therapy for obstructive sleep apnea-related hypertension and renal injury.

  6. Cardiac autonomic nerve distribution and arrhythmia

    Institute of Scientific and Technical Information of China (English)

    Quan Liu; Dongmei Chen; Yonggang Wang; Xin Zhao; Yang Zheng

    2012-01-01

    OBJECTIVE: To analyze the distribution characteristics of cardiac autonomic nerves and to explore the correlation between cardiac autonomic nerve distribution and arrhythmia.DATA RETRIEVAL: A computer-based retrieval was performed for papers examining the distribution of cardiac autonomic nerves, using "heart, autonomic nerve, sympathetic nerve, vagus nerve, nerve distribution, rhythm and atrial fibrillation" as the key words.SELECTION CRITERIA: A total of 165 studies examining the distribution of cardiac autonomic nerve were screened, and 46 of them were eventually included.MAIN OUTCOME MEASURES: The distribution and characteristics of cardiac autonomic nerves were observed, and immunohistochemical staining was applied to determine the levels of tyrosine hydroxylase and acetylcholine transferase (main markers of cardiac autonomic nerve distribution). In addition, the correlation between cardiac autonomic nerve distribution and cardiac arrhythmia was investigated.RESULTS: Cardiac autonomic nerves were reported to exhibit a disordered distribution in different sites, mainly at the surface of the cardiac atrium and pulmonary vein, forming a ganglia plexus. The distribution of the pulmonary vein autonomic nerve was prominent at the proximal end rather than the distal end, at the upper left rather than the lower right, at the epicardial membrane rather than the endocardial membrane, at the left atrium rather than the right atrium, and at the posterior wall rather than the anterior wall. The main markers used for cardiac autonomic nerves were tyrosine hydroxylase and acetylcholine transferase. Protein gene product 9.5 was used to label the immunoreactive nerve distribution, and the distribution density of autonomic nerves was determined using a computer-aided morphometric analysis system.CONCLUSION: The uneven distribution of the cardiac autonomic nerves is the leading cause of the occurrence of arrhythmia, and the cardiac autonomic nerves play an important role in the

  7. Nerve biopsy

    Science.gov (United States)

    Biopsy - nerve ... A nerve biopsy is most often done on a nerve in the ankle, forearm, or along a rib. The health care ... feel a prick and a mild sting. The biopsy site may be sore for a few days ...

  8. Prejunctional inhibition of sympathetically evoked pupillary dilation in cats by activation of histamine H3 receptors.

    Science.gov (United States)

    Koss, M C; Hey, J A

    1993-08-01

    Frequency-dependent pupillary dilations were evoked by electrical stimulation of the pre- or post-ganglionic cervical sympathetic nerve (sympatho-excitation) or the hypothalamus (parasympatho-inhibition) in sympathectomized anesthetized cats. Systemic administration of the selective histamine H3 receptor agonist (R)-alpha-methylhistamine (R alpha MeHA) produced a dose-dependent depression of mydriasis due to direct neural sympathetic activation but had no effect on responses elicited by parasympathetic withdrawal. The histamine H2 receptor agonist, dimaprit, was inactive. R alpha MeHA was much more effective in depressing sympathetic responses obtained at lower frequencies when compared to higher frequencies of stimulation. Responses evoked both pre- and postganglionically were inhibited by R alpha MeHA. This peripheral sympatho-inhibitory action of R alpha MeHA was antagonized by the histamine H3 receptor blocker thioperamide but not by intravenous pretreatment with the histamine H1 receptor antagonist chlorpheniramine. Histamine H2 receptor blockers cimetidine and ranitidine were also without effect. R alpha MeHA did not depress pupillary responses elicited by i.v. (-)-adrenaline. The results demonstrate that histamine H3 receptors modulate sympathetic activation of the iris at a site proximal to the iris dilator muscle. The predominant mechanism of action appears to the prejunctional inhibition of noradrenaline release from postganglionic sympathetic nerve endings. However, a concomitant ganglionic inhibitory action cannot be excluded.

  9. Degenerative pathological irritations to cervical PLL may play a role in presenting sympathetic symptoms.

    Science.gov (United States)

    Wang, Zhanchao; Wang, Xinwei; Yuan, Wen; Jiang, Dongjie

    2011-11-01

    The mechanism of cervical vertigo remains unknown. Stimulation of arterial vertebralis caused by osteophyte of the Luschka joint or segmental instability of the cervical spine was considered to be a potential factor contributing to it. Years of studies found that the ischemia of the vertebral artery is not directly correlated with the clinical symptoms of vertigo, and can not be used to explain cervical vertigo as a sole reason. As proven by clinical practical experience, the routine anterior cervical decompression and fusion (ACDF) procedure, in which the degenerative disc and posterior longitudinal ligament (PLL) were often removed, shows positive results for elimination of the sympathetic symptoms. In this article, we hypothesize that: (1) there are sympathetic nerve postganglionic fibers distributed in the PLL or discs; (2) pathological changes secondary to degeneration of the intervertebral disc may cause irritation of sympathetic nerve fibers in PLL or discs, leading to sympathetic symptoms via certain pathways; (3) removal of the PLL or stabilization of the segment which decreases the irritation to PLL will help to eliminate the sympathetic symptoms. Copyright © 2011. Published by Elsevier Ltd.

  10. Central exogenous nitric oxide decreases cardiac sympathetic drive and improves baroreflex control of heart rate in ovine heart failure.

    Science.gov (United States)

    Ramchandra, Rohit; Hood, Sally G; May, Clive N

    2014-08-01

    Heart failure (HF) is associated with increased cardiac and renal sympathetic drive, which are both independent predictors of poor prognosis. A candidate mechanism for the centrally mediated sympathoexcitation in HF is reduced synthesis of the inhibitory neuromodulator nitric oxide (NO), resulting from downregulation of neuronal NO synthase (nNOS). Therefore, we investigated the effects of increasing the levels of NO in the brain, or selectively in the paraventricular nucleus of the hypothalamus (PVN), on cardiac sympathetic nerve activity (CSNA) and baroreflex control of CSNA and heart rate in ovine pacing-induced HF. The resting level of CSNA was significantly higher in the HF than in the normal group, but the resting level of RSNA was unchanged. Intracerebroventricular infusion of the NO donor sodium nitroprusside (SNP; 500 μg · ml(-1)· h(-1)) in conscious normal sheep and sheep in HF inhibited CSNA and restored baroreflex control of heart rate, but there was no change in RSNA. Microinjection of SNP into the PVN did not cause a similar cardiac sympathoinhibition in either group, although the number of nNOS-positive cells was decreased in the PVN of sheep in HF. Reduction of endogenous NO with intracerebroventricular infusion of N(ω)-nitro-l-arginine methyl ester decreased CSNA in normal but not in HF sheep and caused no change in RSNA in either group. These findings indicate that endogenous NO in the brain provides tonic excitatory drive to increase resting CSNA in the normal state, but not in HF. In contrast, exogenously administered NO inhibited CSNA in both the normal and HF groups via an action on sites other than the PVN. Copyright © 2014 the American Physiological Society.

  11. Bradykinin Contributes to Sympathetic and Pressor Responses Evoked by Activation of Skeletal Muscle Afferents P2X in Heart Failure

    Directory of Open Access Journals (Sweden)

    Jihong Xing

    2016-11-01

    Full Text Available Background/Aims: Published data suggest that purinergic P2X receptors of muscle afferent nerves contribute to the enhanced sympathetic nervous activity (SNA and blood pressure (BP responses during static exercise in heart failure (HF. In this study, we examined engagement of bradykinin (BK in regulating responses of SNA and BP evoked by P2X stimulation in rats with HF. We further examined cellular mechanisms responsible for BK. We hypothesized that BK potentiates P2X currents of muscle dorsal root ganglion (DRG neurons, and this effect is greater in HF due to upregulation of BK kinin B2 and P2X3 receptor. As a result, BK amplifies muscle afferents P2X-mediated SNA and BP responses. Methods: Renal SNA and BP responses were recorded in control rats and rats with HF. Western Blot analysis and patch-clamp methods were employed to examine the receptor expression and function of DRG neurons involved in the effects of BK. Results: BK injected into the arterial blood supply of the hindlimb muscles heightened the reflex SNA and BP responses induced by P2X activation with α,β-methylene ATP to a greater degree in HF rats. In addition, HF upregulated the protein expression of kinin B2 and P2X3 in DRG and the prior application of BK increased the magnitude of α,β-methylene ATP-induced currents in muscle DRG neurons from HF rats. Conclusion: BK plays a facilitating role in modulating muscle afferent P2X-engaged reflex sympathetic and pressor responses. In HF, P2X responsivness is augmented due to increases in expression of kinin B2 and P2X3 receptors and P2X current activity.

  12. Sympathetic innervation of the spleen in male Brown Norway rats: a longitudinal aging study.

    Science.gov (United States)

    Perez, Sam D; Silva, Dorian; Millar, Ashley Brooke; Molinaro, Christine A; Carter, Jeff; Bassett, Katie; Lorton, Dianne; Garcia, Paola; Tan, Laren; Gross, Jonathon; Lubahn, Cheri; Thyagarajan, Srinivasan; Bellinger, Denise L

    2009-12-11

    Aging leads to reduced cellular immunity with consequent increased rates of infectious disease, cancer, and autoimmunity in the elderly. The sympathetic nervous system (SNS) modulates innate and adaptive immunity via innervation of lymphoid organs. In aged Fischer 344 (F344) rats, noradrenergic (NA) nerve density in secondary lymphoid organs declines, which may contribute to immunosenescence with aging. These studies suggest there is SNS involvement in age-induced immune dysregulation. The purpose of this study was to longitudinally characterize age-related change in sympathetic innervation of the spleen and sympathetic activity/tone in male Brown Norway (BN) rats, which live longer and have a strikingly different immune profile than F344 rats, the traditional animal model for aging research. Splenic sympathetic neurotransmission was evaluated between 8 and 32 months of age by assessing (1) NA nerve fiber density, (2) splenic norepinephrine (NE) concentration, and (3) circulating catecholamine levels after decapitation. We report a decline in NA nerve density in splenic white pulp (45%) at 15 months of age compared with 8-month-old (M) rats, which is followed by a much slower rate of decline between 24 and 32 months. Lower splenic NE concentrations between 15 and 32 months of age compared with 8M rats were consistent with morphometric findings. Circulating catecholamine levels after decapitation stress generally dropped with increasing age. These findings suggest there is a sympathetic-to-immune system dysregulation beginning at middle age. Given the unique T-helper-2 bias in BN rats, altered sympathetic-immune communication may be important for understanding the age-related rise in asthma and autoimmunity.

  13. Enhanced Blood Pressure–Lowering Effect of Olmesartan in Hypertensive Patients With Chronic Kidney Disease–Associated Sympathetic Hyperactivity: HONEST Study

    Science.gov (United States)

    Kario, Kazuomi; Saito, Ikuo; Kushiro, Toshio; Teramukai, Satoshi; Mori, Yoshihiro; Hiramatsu, Katsutoshi; Kobayashi, Fumiaki; Shimada, Kazuyuki

    2013-01-01

    To investigate the blood pressure (BP)–lowering effect of olmesartan in relation to chronic kidney disease (CKD)–associated sympathetic nerve activity, a subanalysis was performed using data from the first 16 weeks of the Home BP Measurement With Olmesartan-Naive Patients to Establish Standard Target Blood Pressure (HONEST) study, a prospective observational study of hypertensive patients. Essential hypertensive patients who took no antihypertensive agent at baseline were classified based on baseline morning home systolic BP (MHSBP) in quartiles. In each class, patients were further classified based on baseline morning home pulse rate (MHPR). A subgroup analysis in patients with/without chronic kidney disease (CKD) was performed. A total of 5458 patients (mean age, 63.0 years; 51.6% women) were included. In the 4th quartile of baseline MHSBP (≥165 mm Hg), patients with MHPR ≥70 beats per minute had a greater BP reduction (by 3.2 mm Hg) than those with MHPR olmesartan-based treatment (P=.0005). An even greater BP reduction (by 6.6 mm Hg) was observed in patients with CKD than in patients without CKD in this group (P=.0084). Olmesartan was more effective in hypertensive patients with high MHSBP and MHPR ≥70 beats per minute, especially in patients with CKD. Olmesartan may have enhanced BP-lowering effects by improving renal ischemia in hypertensive CKD patients with potential increased sympathetic nerve activity. PMID:23889717

  14. Mineralocorticoid receptors, inflammation and sympathetic drive in a rat model of systolic heart failure.

    Science.gov (United States)

    Felder, Robert B

    2010-01-01

    Appreciation for the role of aldosterone and mineralocorticoid receptors in cardiovascular disease is accelerating rapidly. Recent experimental work has unveiled a strong relationship between brain mineralocorticoid receptors and sympathetic drive, an important determinant of outcome in heart failure and hypertension. Two putative mechanisms are explored in this manuscript. First, brain mineralocorticoid receptors may influence sympathetic discharge by regulating the release of pro-inflammatory cytokines into the circulation. Blood-borne pro-inflammatory cytokines act upon receptors in the microvasculature of the brain to induce cyclooxygenase-2 activity and the production of prostaglandin E(2), which penetrates the blood-brain barrier to activate the sympathetic nervous system. Second, brain mineralocorticoid receptors may influence sympathetic drive by upregulating the activity of the brain renin-angiotensin system, resulting in NAD(P)H oxidase-dependent superoxide production. A potential role for superoxide-dependent mitogen-activated protein kinase signalling pathways in the regulation of sympathetic nerve activity is also considered. Other potential downstream signalling mechanisms contributing to mineralocorticoid receptor-mediated sympathetic excitation are under investigation.

  15. Reduced sympathetic neurite outgrowth on uterine tissue sections from rats treated with estrogen.

    Science.gov (United States)

    Richeri, Analía; Bianchimano, Paola; Crutcher, Keith A; Brauer, M Mónica

    2010-05-01

    In order to evaluate the contribution of substrate-bound factors to the extent and patterning of the sympathetic innervation of rat uterus following estrogen treatment, superior cervical ganglion explants from neonatal and adult ovariectomized rats were cultured on tissue sections of fresh frozen uterus from adult ovariectomized rats treated with estrogen or a vehicle. The main findings were: (1) neurite growth was greatly influenced by histological features of the underlying section; (2) on myometrial sections, neurites followed the orientation of the main axis of the longitudinally sectioned muscle cells; (3) neurites showed limited growth on transversally sectioned smooth muscle; (4) neuritic patterning was unaffected by a reduction in migrating ganglionic non-neuronal cells; (5) neurite outgrowth, but not non-neural cell migration, was markedly reduced on myometrial sections from rats treated with estrogen. These results suggest that adult myometrium continues to provide signals allowing the organotypic patterning and growth of sympathetic axons, that estrogen treatment modifies myometrial substrate properties so that it is less supportive for sympathetic neurite growth, and that adult sympathetic neurons retain their ability to recognize substrate-bound cues present in the myometrium. On endometrial sections, neurites formed radially symmetric halos, which were reduced in size on estrogen-treated endometrial substrates. Thus, changes in the neuritogenic capacity of the uterus underlie plasticity in uterine sympathetic nerves, and alterations in substrate-bound factors contribute to the diminished receptivity of the estrogenized uterus to its sympathetic innervation.

  16. Imaging of the autonomic nervous system: focus on cardiac sympathetic innervation.

    Science.gov (United States)

    Goldstein, David S

    2003-12-01

    Symptoms or signs of abnormal autonomic nervous system function occur commonly in several neurological disorders. Clinical evaluations have depended on physiological, pharmacological, and neurochemical approaches. Recently, imaging of sympathetic noradrenergic innervation has been introduced and applied especially in the heart. Most studies have used the radiolabeled sympathomimetic amine, (123)I-metaiodobenzylguanidine. Decreased uptake or increased "washout" of (123)I-metaiodobenzylguanidine-derived radioactivity is associated with worse prognosis or more severe disease in hypertension, congestive heart failure, arrhythmias, and diabetes mellitus. This pattern may reflect a high rate of postganglionic sympathetic nerve traffic to the heart. Many recent studies have agreed on the remarkable finding that all patients with Parkinson's disease and orthostatic hypotension have a loss of cardiac sympathetic innervation, whereas all patients with multiple system atrophy, often difficult to distinguish clinically from Parkinson's disease, have intact cardiac sympathetic innervation. Because Parkinson's disease entails a postganglionic sympathetic noradrenergic lesion, the disease appears to be not only a movement disorder, with dopamine loss in the nigrostriatal system of the brain, but also a dysautonomia, with noradrenaline loss in the sympathetic nervous system of the heart. As new ligands are developed, one may predict further discoveries of involvement of components of the autonomic nervous system in neurological diseases.

  17. Comparison of 2% mepivacaine, clipping, and radiofrequency thermocoagulation for duration and magnitude of action in peripheral arterial blood flow induced by sympathetic block in anesthetized dogs.

    Science.gov (United States)

    Otani, Taro; Shinozaki, Mio; Takahashi, Yoshiyuki; Ikeda, Tomohito; Kimura, Yoshiyuki; Nagao, Masaru; Yamaguchi, Shigeki; Kitajima, Toshimitsu

    2010-01-01

    Thoracic sympathetic block has recently been performed by placement of the clips on the sympathetic chain to interrupt nerve conduction. The aim of this study was to compare clipping with 2% mepivacaine and radiofrequency thermocoagulation for the potency of sympathetic block from the results of the duration and magnitude of the vasodilation effect induced by thoracic sympathetic block in dogs. We measured mean arterial pressure, heart rate, and right and left brachial artery blood flow (BABF) before and after thoracic sympathetic block in 24 dogs. The experimental protocol was designed as follows: (1) left thoracic sympathetic block by 1.0 mL of 2% mepivacaine (n = 8), (2) left thoracic sympathetic block by clipping (n = 8), and (3) left thoracic sympathetic block by radiofrequency thermocoagulation (n = 8). Mean arterial pressure and heart rate did not change significantly throughout the study in either group. Left thoracic sympathetic block by 2% mepivacaine increased left BABF significantly from 5 to 70 mins after the block (baseline, 100%; peak at 10 mins after the block, 179% ± 33%; P mepivacaine and a less potency compared with radiofrequency thermocoagulation in thoracic sympathetic block in dogs.

  18. Intrarenal artery injection of capsaicin activates spontaneous activity of renal afferent nerve fibers%肾动脉内注射辣椒素兴奋肾神经传入纤维的自发活动

    Institute of Scientific and Technical Information of China (English)

    马慧娟; 武宇明; 马会杰; 张丽华; 何瑞荣

    2003-01-01

    The effects of intrarenal artery injection of capsaicin on multi- and single-unit spontaneous discharges of renal afferent nerve fibers were investigated in anesthetized rabbits. The results obtained are as follows: ( 1 ) intrarenal artery injection of capsaicin (20, 40, and 60 nmol/kg) increased the renal afferent nerve activity (ARNA) in a dose-dependent manner with unchanged arterial pressure; (2) pretreatment with ruthenium red (40 mmol/kg), a capsaicin receptor antagonist, completely abolished the effect of capsaicin; and (3) pretreatment with a nitric oxide synthase inhibitor L-NAME ( N6-nitro-L-arginine methylester, 0. 1 mmol/kg), significantly enhanced the ARNA response to capsaicin. The results suggest that intrarenal artery injection of capsaicin can activate ARNA via capsaicin receptors in anesthetized rabbits and that nitric oxide may be involved in regulating the activity of renal sensory nerve fibers as an inhibitory neurotransmitter.%应用记录肾传入神经多单位和单位放电的方法,观察肾动脉内注射辣椒素对麻醉家兔肾神经传入纤维自发放电活动的影响.结果表明:(1)肾动脉内注射辣椒素20、40和60nmol/kg可呈剂量依赖性地兴奋肾传入纤维的活动,而动脉血压不变;(2)静脉内预先应用辣椒素受体阻断剂钌红(40 mmok/kg),可完全阻断辣椒素对肾传入纤维的兴奋作用.(3)静脉内预先注射一氧化氮合酶抑制剂L-NAME(0.1 mmo/kg),能延长并增强肾传入神经对辣椒素的反应.以上结果提示:肾动脉内应用辣椒素可兴奋肾传入纤维的自发放电活动.一氧化氮作为抑制因素参与辣椒素诱导的肾传入神经兴奋.

  19. 比索洛尔联合音乐疗法对原发性高血压患者静息心率及交感神经活性的影响%Effect of Bisoprolol Combined with Music Therapy for Stabilizing Resting Heart Rate and Sympathetic Nerve Activity in Essential Hypertension Patients

    Institute of Scientific and Technical Information of China (English)

    唐雪敏; 景颖颖

    2015-01-01

    Objective To observe the effect of bisoprolol combined with the music therapy for stabilizing the resting heart rate and sym-pathetic nerve activity in the patients with essential hypertension. Methods Totally 186 patients with essential hypertension were randomly divided into the control group,observation group 1 and observation group 2,62 cases in each group. The control group was treated by Amlodipine Besylate Tablets,the observation group 1 was added with bisoprolol on the basis of the control group and the observation group 2 was combined with the music therapy on the basis of the observation group 1. The treatment in 3 groups lasted for 30 d. Results The systolic and diastolic blood pressure of the 3 groups were significantly decreased than before treatment( P < 0. 05),but there was no statistically significant difference among 3 groups( P ? 0. 05). The decrease of resting heart rate after treatment in the con-trol group was unobvious compared with before treatment( P ? 0. 05),but which in the observation group 1 and 2 were obvious,the dif-ference was statistically significant( P < 0. 05);the decrease in the observation group 2 was more significant than that in the observation group 1( P < 0. 05). The plasma norepinephrine,renin and angiotensin Ⅱlevels after treatment in the observation group 1 and 2 were decreased significantly( P < 0. 05),but only plasma norepinephrine and renin levels in the control group were decreased( P < 0. 05),the angiotensin Ⅱlevel had no significant change( P ? 0. 05);in the comparison among groups,the 3 indexes levels in the observation group 1 and 2 were lower than those in the control group,moreover the decrease in the observation group 2 was more significant than that in the observation group 1( P < 0. 05). The occurrence rate of adverse reactions during the treatment process had no significant differences among 3 groups. Conclusion Bisoprolol combined with the music therapy in the treatment process of essential hypertension

  20. 肾去交感神经对心房神经节刺激诱发心房颤动的影响%Effect of renal sympathetic denervation on the inducibility of atrial fibrillation by anterior right ganglionic plexi stimulation

    Institute of Scientific and Technical Information of China (English)

    于胜波; 代子玄; 邹明辉; 王徐乐; 肖金平; 赵庆彦; 黄从新

    2013-01-01

    Objective To investigate the effect of renal sympathetic denervation on inducibility of atrial fibrillation(AF) by anterior right ganglionic plexi (ARGP)stimulation.Methods Thirteen dogs were used for the study as follows:control group(n =7) and renal artery ablation (RAA) group (n =6).In control group,after right thoracotomy,high-frequency electrical stimulation(20 Hz,0.1 ms duration)was applied to the ARGP for 1 minute by incremental voltages up to the voltage that induced AF.In RAA group,after atrial effective refractory period (AERP) measured,each renal artery was ablated and dogs were raised for 6 weeks.The procedure of ARGP stimulation was same as in the control group.Blood was collected before and after ablation 6 weeks to measure the levels ofangiotensin Ⅱ(Ang Ⅱ)and aldosterone(ALD) in RAA dogs.Results AERP had no significant change before and after renal artery ablation 6 weeks [(134.4±19.2) ms vs (142.0±21.5) ms,P>0.05].Compared with that in control group,dogs had higher voltage in the sinus rate slowing response induced by ARGP stimulation in RAA group[(3.5±1.6)V vs(1.6±0.3)V,P=0.03].Furthermore,the lowest voltage that induce AF was higher in RAA group than that in control group[(5.1±1.0)V vs(2.1±0.7)V,P=0.03].The plasma Ang Ⅱ and aldosterone concentration showed a greatly decreasing after RAA 6 weeks in RAA group [Ang Ⅱ:(142.8±31.7) pg/ml vs(91.7±23.8)pg/ml,P=0.01 ; Aldosterone:(272.2±37.4) pg/ml vs(156.3±17.6)pg/ml,P<0.01].Conclusions Renal sympathetic denervation inhibited the inducibility of AF during ARGP stimulation.This effect might have relationship with decreased activity of renin-angiotensin-aldosterone system(RAAS).%目的 探讨经导管消融肾交感神经后对心房右前神经节(ARGP)刺激诱发心房颤动(房颤)的影响.方法 13只犬随机分为对照组(n=7)和消融组(n=6).对照组犬于右侧第4肋间开胸,采用不同电压高频刺激(20 Hz,0.1 ms) ARGP,观察心率减慢和房颤诱发情况;消

  1. Renal Denervation for Chronic Heart Failure: Background and Pathophysiological Rationale.

    Science.gov (United States)

    Böhm, Michael; Ewen, Sebastian; Mahfoud, Felix

    2017-01-01

    The activation of the sympathetic nervous system is associated with cardiovascular hospitalizations and death in heart failure. Renal denervation has been shown to effectively reduce sympathetic overdrive in certain patients with uncontrolled hypertension. Pilot trials investigating renal denervation as a potential treatment approach for heart failure were initiated. Heart failure comorbidities like obstructive sleep apnea, metabolic syndrome and arrhythmias could also be targets for renal denervation, because these occurrences are also mediated by the activation of the sympathetic nervous system. Therefore, renal denervation in heart failure is worthy of further investigation, although its effectiveness still has to be proven. Herein, we describe the pathophysiological rationale and the effect of renal denervation on surrogates of the heart failure syndrome.

  2. Sympathetic nervous system promotes hepatocarcinogenesis by modulating inflammation through activation of alpha1-adrenergic receptors of Kupffer cells.

    Science.gov (United States)

    Huan, Hong-Bo; Wen, Xu-Dong; Chen, Xue-Jiao; Wu, Lin; Wu, Li-Li; Zhang, Liang; Yang, Da-Peng; Zhang, Xia; Bie, Ping; Qian, Cheng; Xia, Feng

    2017-01-01

    The sympathetic nervous system (SNS) is known to play a significant role in tumor initiation and metastasis. Hepatocellular carcinoma (HCC) frequently occurs in cirrhotic livers after chronic inflammation, and the SNS is hyperactive in advanced liver cirrhosis. However, it remains unclear whether the SNS promotes hepatocarcinogenesis by modulating chronic liver inflammation. In this study, a retrospective pathological analysis and quantification of sympathetic nerve fiber densities (tyrosine hydroxylase, TH(+)) in HCC patients, and diethylnitrosamine (DEN)-induced hepatocarcinogenesis in rats were performed. Our data showed that high density of sympathetic nerve fibers and α1-adrenergic receptors (ARs) of Kupffer cells (KCs) were associated with a poor prognosis of HCC. Sympathetic denervation or blocking of α1-ARs decreased DEN-induced HCC incidence and tumor development. In addition, synergistic effects of interleukin-6 (IL-6) and transforming growth factor-beta (TGF-β) in hepatocarcinogenesis were observed. The suppression of the SNS reduced IL-6 and TGF-β expression, which suppressed hepatocarcinogenesis, and KCs play a key role in this process. After the ablation of KCs, IL-6 and TGF-β expression and the development of HCC were inhibited. This study demonstrates that sympathetic innervation is crucial for hepatocarcinogenesis and that the SNS promotes hepatocarcinogenesis by activating α1-ARs of KCs to boost the activation of KCs and to maintain the inflammatory microenvironment. These results indicate that sympathetic denervation or α1-ARs blockage may represent novel treatment approaches for HCC.

  3. Estrogen up-regulation of semaphorin 3F correlates with sympathetic denervation of the rat uterus.

    Science.gov (United States)

    Richeri, Analía; Chalar, Cora; Martínez, Gaby; Greif, Gonzalo; Bianchimano, Paola; Brauer, M Mónica

    2011-10-28

    Current evidence indicates that rises in systemic levels of estrogen create in the uterus an inhibitory environment for sympathetic nerves. However, molecular insights of these changes are far from complete. We evaluated if semaphorin 3F mRNA, a sympathetic nerve repellent, was produced by the rat uterus and if its expression was modulated by estrogen. We also analyzed whether uterine nerves express the semaphorin 3F binding receptor, neuropilin-2. Uterine levels of semaphorin 3F mRNA were measured using real time reverse transcriptase-polymerase chain reaction in prepubertal rat controls and following chronic estrogen treatment. Localization of semaphorin 3F transcripts was determined by in situ hybridization and the expression of neuropilin-2 was assessed by immunohistochemistry. These studies showed that: (1) chronic estrogen treatment led to a 5-fold induction of semaphorin 3F mRNA in the immature uterus; (2) estrogen provoked a tissue-specific induction of semaphorin 3F which was particularly localized in the connective tissue that borders muscle bundles and surrounds intrauterine blood vessels; (3) two major cell-types were recognized in the areas where transcripts were concentrated, fibroblast-like cells and infiltrating eosinophil leukocytes; and (4) some delicate nerve terminal profiles present in the estrogenized uterus were immunoreactive for neuropilin-2. Temporal and spatial expression patterns of semaphorin 3F/neuropilin-2 are consistent with a possible role of this guidance cue in the remodeling of uterine sympathetic innervation by estrogen. Though correlative in its nature, these data support a model whereby semaphorin 3F, in combination with other inhibitory molecules, converts the estrogenized myometrium to an inhospitable environment for sympathetic nerves.

  4. Neurophysiological analysis of target-related sympathetic pathways--from animal to human: similarities and differences.

    Science.gov (United States)

    Jänig, W; Häbler, H-J

    2003-03-01

    The sympathetic nervous system regulates many different target tissues in the somatic and visceral domains of the body in a differentiated manner, indicating that there exist separate sympathetic pathways that are functionally defined by their target cells. Signals generated by central integration and channelled through the preganglionic neurons into the final sympathetic pathways are precisely transmitted through the para- and prevertebral ganglia and at the neuroeffector junctions to the effector cells. Neurophysiological recordings of activity in postganglionic neurons in skin and muscle nerves using microneurography in human subjects and in skin, muscle and visceral nerves, using conventional recording techniques in anaesthetized animals, clearly show that each type of sympathetic neuron exhibits a discharge pattern that is characteristic for its target cells and, therefore, its function. These findings justify labelling the neurons as muscle vasoconstrictor, cutaneous vasoconstrictor, sudomotor, lipomotor, cardiomotor, secretomotor neurons, etc. The discharge patterns monitor aspects of the central organization of the respective sympathetic system in the neuraxis and forebrain. They can be dissected into several distinct reflexes (initiated by peripheral and central afferent inputs) and reactions connected to central signals (related to respiration, circadian and other rhythms, command signals generated in the forebrain, etc). They are functional markers for the sympathetic final pathways. These neurophysiological recordings of the discharge patterns from functionally identified neurons of sympathetic pathways in the human and in animals are the ultimate reference for all experimental investigations that aim to unravel the central organization of the sympathetic systems. The similarities of the results obtained in the in vivo studies in the human and in animals justify concluding that the principles of the central organization of sympathetic systems are

  5. Sympathetic neural control of indoleamine metabolism in the rat pineal gland

    Science.gov (United States)

    Lynch, H. J.; Hsuan, M.; Wurtman, R. J.

    1975-01-01

    The mechanisms responsible for the acceleration in rat pineal biosynthetic activity in response to prolonged exposure to darkness or to immobilization were investigated in animals whose pineals were surgically denervated. Some animals were adrenalectomized to remove one potential source of circulating catecholamines, and some were subjected to a partial chemical sympathectomy accomplished by a series of intravenous injections of 6-hydroxydopamine. Results suggest that N-acetyltransferase (NAT) activity can be enhanced either by release of norepinephrine from sympathetic terminals within the pineal or from sympathetic nerve terminals elsewhere. The stress of immobilization stimulates the pineal by increasing circulating catecholamines. Photic control of pineal function requires intact pineal sympathetic innervation, since the onset of darkness apparently does not cause a sufficient rise in circulating catecholamines to stimulate the pineal. The present studies suggest that nonspecific stress triggers increased biosynthesis and secretion of melatonin; it is possible that this hormone may participate in mechanisms of adaptation.

  6. The explore of mechanism,validity and safety of renal sympathetic denervation for hypertensive dogs%去肾脏交感神经术对犬高血压的影响机制及有效性、安全性探讨

    Institute of Scientific and Technical Information of China (English)

    赵斌; 卢成志; 张欣

    2012-01-01

    目的:通过去肾脏交感神经术(RSD)对犬高血压的治疗,探讨高血压与肾素-血管紧张素-醛固酮系统(RAS)的关系,并评估RSD的有效性与安全性.方法:18只杂种狗随机分为干预组(n=10)和对照组(n=8)两组,干预组为高血压造模组,两组实验动物都接受RSD.观察的主要指标是平均动脉压(MAP)的变化,分别在术前和术后2、4、10周监测血压,同时在术后第2、6、10周监测肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)、肌酐(Cr)等指标,通过对这些数据进行方差分析,来评价RSD的有效性与安全性.结果:在干预组,造模后MAP增高明显,由(134.4±4.32)mmHg升至(153.8±7.2)mmHg(P<0.001);在行RSD治疗后,MAP在2、4和10周后分别降至(137.6±8.46)mmHg、(132.3±6.20)mmHg和(125.5±2.87)mmHg,同时PRA、AngⅡ、ALD水平都较术前下降(P<0.05),Cr水平无明显变化(P>0.05).结论:RAS在高血压的发生和发展过程中发挥着重要的作用,RSD能够产生显著和持久的血压下降作用,能有效降低RAS的活性,并且手术过程没有造成严重肾功能受损.%Objective To explore the treatment of renal sympathetic denervation (RSD) for hypertension and assess the validity of the treatment, discussing the relation between hypertension and renin-angiotensin-aldosterone system(RAS) at the same time. Methods Eighteen mongrel dogs were studied as intervention (re = 10) and control (n= 8) groups, Ihe intervention group was made the neurogenic hypertension model, Iwo groups were received RSD. Primary endpoints were changes of mean blood pressure before and at 2,4 and 10 weeks after procedure. We assessed the effectiveness of renal sympathetic denervation with renin activity (PRA), angiotensin II (Ang II ), aldosterone(ALD), and creatinine(Cr) in the intervention group. The changes of PRA, Ang II , ALD, and Cr were detected at 2, 6 and 10 weeks after procedure. We assessed the data changes effectiveness by repeated measures

  7. Sympathetic Innervation Induced in Engrafted Engineered Cardiomyocyte Sheets by Glial Cell Line Derived Neurotrophic Factor In Vivo

    Directory of Open Access Journals (Sweden)

    Xian-ming Fu

    2013-01-01

    Full Text Available The aim of myocardial tissue engineering is to repair or regenerate damaged myocardium with engineered cardiac tissue. However, this strategy has been hampered by lack of functional integration of grafts with native myocardium. Autonomic innervation may be crucial for grafts to function properly with host myocardium. In this study, we explored the feasibility of in vivo induction of autonomic innervation to engineered myocardial tissue using genetic modulation by adenovirus encoding glial cell line derived neurotrophic factor (GDNF. GFP-transgene (control group or GDNF overexpressing (GDNF group engineered cardiomyocyte sheets were transplanted on cryoinjured hearts in rats. Nerve fibers in the grafts were examined by immunohistochemistry at 1, 2, and 4 weeks postoperatively. Growth associated protein-43 positive growing nerves and tyrosine hydroxylase positive sympathetic nerves were first detected in the grafts at 2 weeks postoperatively in control group and 1 week in GDNF group. The densities of growing nerve and sympathetic nerve in grafts were significantly increased in GDNF group. No choline acetyltransferase immunopositive parasympathetic nerves were observed in grafts. In conclusion, sympathetic innervation could be effectively induced into engrafted engineered cardiomyocyte sheets using GDNF.

  8. Sympathetic crashing acute pulmonary edema.

    Science.gov (United States)

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-12-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence.

  9. Radionuclide imaging of cardiac sympathetic innervation in heart failure: unlocking untapped potential.

    Science.gov (United States)

    Gupta, Shuchita; Amanullah, Aman

    2015-03-01

    Heart failure (HF) is associated with sympathetic overactivity, which contributes to disease progression and arrhythmia development. Cardiac sympathetic innervation imaging can be performed using radiotracers that are taken up in the presynaptic nerve terminal of sympathetic nerves. The commonly used radiotracers are (123)I-metaiodobenzylguanidine ((123)I-mIBG) for planar and single-photon emission computed tomography imaging, and (11)C-hydroxyephedrine for positron emission tomography imaging. Sympathetic innervation imaging has been used in assessing prognosis, response to treatment, risk of ventricular arrhythmias and sudden death and prediction of response to cardiac resynchronization therapy in patients with HF. Other potential applications of these techniques are in patients with chemotherapy-induced cardiomyopathy, predicting myocardial recovery in patients with left ventricular assist devices, and assessing reinnervation following cardiac transplantation. There is a lack of standardization with respect to technique of (123)I-mIBG imaging that needs to be overcome for the imaging modality to gain popularity in clinical practice.

  10. Sensory and sympathetic innervation of cervical facet joint in rats

    Institute of Scientific and Technical Information of China (English)

    ZHOU Hai-yu; CHEN An-min; GUO Feng-jing; LIAO Guang-jun; XIAO Wei-dong

    2006-01-01

    sympathetic ganglions through nerve fibers outside the central nerve system.

  11. Mechanism of renal effects of intracerebroventricular histamine in rabbits.

    Science.gov (United States)

    Kook, Y J; Kim, K K; Yang, D K; Ahn, D S; Choi, B K

    1988-01-01

    Histamine, when given intracerebroventricularly (i.c.v.), has been reported to produce antidiuresis in the rabbit. In this study it was attempted to elucidate the mechanism involved in the effect. Histamine (H), 100 micrograms/kg i.c.v., produced antidiuresis with decreases in renal plasma flow and glomerular filtration rate in urethane-anesthetized rabbits. With larger doses, a tendency towards increased electrolyte excretion was noted in spite of decreased filtration. In the denervated kidney, marked diuresis and natriuresis were observed following i.c.v. H, whereas the contralateral innervated kidney responded with typical antidiuresis. Reserpinized rabbits also responded with marked natriuresis to i.c.v. H. Diphenhydramine (D), 250 micrograms/kg i.c.v., increased urine flow rate, sodium and potassium excretion, along with increase in renal perfusion. With 750 micrograms/kg i.c.v., marked natriuresis was observed in spite of decreased filtration. When H was given after D (250 micrograms/kg) the antidiuresis was completely abolished, and diuresis became more prominent. Cimetidine, 250 micrograms/kg i.c.v., elicited antidiuresis with decreases in renal hemodynamics, the pretreatment with cimetidine did not influence the antidiuresis by H and no natriuresis was noted. The present study suggests that histamine, given i.c.v., influences renal function in dual ways, i.e., antidiuresis by increasing the sympathetic tone to the kidney and diuresis due to some humoral natriuretic factor, the latter becoming apparent only when the former influence has been removed, and further suggests that H1-receptors might be involved in the nerve-mediated antidiuresis, whereas H2-receptors might mediate the humorally induced natriuresis and diuresis.

  12. Estimated central blood volume in cirrhosis: relationship to sympathetic nervous activity, beta-adrenergic blockade and atrial natriuretic factor

    DEFF Research Database (Denmark)

    Henriksen, Jens Henrik Sahl; Bendtsen, F; Gerbes, A L

    1992-01-01

    The estimated central blood volume (i.e., blood volume in the heart cavities, lungs and central arterial tree) was determined by multiplying cardiac output by circulatory mean transit time in 19 patients with cirrhosis and compared with sympathetic nervous activity and circulating level of atrial...... natriuretic factor. Arterial norepinephrine level, an index of overall sympathetic nervous activity (3.08 nmol/L in patients vs. 1.36 nmol/L in controls; p blood volume (mean = 23 ml/kg in patients vs. 27 ml/kg in controls; p ....05). Similarly, renal venous norepinephrine level (an index of renal sympathetic tone; 4.26 nmol/L in patients vs. 1.78 nmol/L in controls; p blood volume (r = -0.53, n = 18, p

  13. Sympathetic actions on the skeletal muscle.

    Science.gov (United States)

    Roatta, Silvestro; Farina, Dario

    2010-01-01

    The sympathetic nervous system (SNS) modulates several functions in skeletal muscle fibers, including metabolism, ionic transport across the membrane, and contractility. These actions, together with the sympathetic control of other organ systems, support intense motor activity. However, some SNS actions on skeletal muscles may not always be functionally advantageous. Implications for motor control and sport performance are discussed.

  14. Ganglioneuromas involving the hypoglossal nerve and the vagus nerve in a child: Surgical difficulties.

    Science.gov (United States)

    Bakshi, Jaimanti; Mohammed, Abdul Wadood; Lele, Saudamini; Nada, Ritambra

    2016-02-01

    Ganglioneuromas are benign tumors that arise from the Schwann cells of the autonomic nervous system. They are usually seen in the posterior mediastinum and the paraspinal retroperitoneum in relation to the sympathetic chain. In the head and neck, they are usually related to the cervical sympathetic ganglia or to the ganglion nodosum of the vagus nerve or the hypoglossal nerve. We describe what we believe is the first reported case of multiple ganglioneuromas of the parapharyngeal space in which two separate cranial nerves were involved. The patient was a 10-year-old girl who presented with a 2-year history of a painless and slowly progressive swelling on the left side of her neck and a 1-year history hoarseness. She had no history of relevant trauma or surgery. Intraoperatively, we found two tumors in the left parapharyngeal space-one that had arisen from the hypoglossal nerve and the other from the vagus nerve. Both ganglioneuromas were surgically removed, but the affected nerves had to be sacrificed. Postoperatively, the patient exhibited hypoglossal nerve and vocal fold palsy, but she was asymptomatic. In addition to the case description, we discuss the difficulties we faced during surgical excision.

  15. The sympathetic postganglionic and sensory innervation of oviducal magnum in hen: a choleratoxin subunit B-conjugated horseradish peroxidase study

    Science.gov (United States)

    Liu, Jinxiong; Wang, Wenjie; Feng, Yamei; Li, Meiying; Bao, Huijun; Chen, Qiusheng

    2007-01-01

    The anatomy of the extrinsic innervation of the avian magnum has not been accurately demonstrated previously. In the present study, choleratoxin subunit B-conjugated horseradish peroxidase (CB-HRP) was used as a retrograde tracer to determine the sympathetic postganglionic and sensory innervation of the magnum of hens. With regard to the sympathetic postganglionic innervation, following CB-HRP injections under the serosa of the magnum, CB-HRP-positive neurons were found bilaterally in the C12–LS13 ganglia of the sympathetic chain, splanchnic ganglia and adrenal ganglia. The number of labelled neurons in the left ganglia of the sympathetic chain and splanchnic ganglia was approximately 2.1 times that in the right ganglia. This suggests that the unilateral magnum is bilaterally innervated with sympathetic postganglionic nerves, the left nerves being predominant. With regard to the sensory innervation, following tracer injections, CB-HRP-positive neurons were found bilaterally in the spinal ganglia C13–LS12, jugular ganglia and nodose ganglia. The number of positive cells in the left ganglia was about 2.2 times that in the right ganglia. In the spinal ganglia, 85.6% of the labelled neurons were in the T5–LS2 and LS8–LS11 ganglia. These results suggest that the sensory nerve fibres of the magnum reach the central nervous system principally via two groups of spinal ganglia and vagus nerves, and that the innervation is bilateral although the left-hand route predominates. Moreover, 45.7% of all the CB-HRP-labelled neurons were found in the rectal region of the intestinal nerve of Remak (INR), which suggests that the INR plays a very important role in the functional regulation of the magnum. PMID:17328711

  16. Research progress of myocardial ischemia and sympathetic afferent%心肌缺血与交感神经传入的研究进展

    Institute of Scientific and Technical Information of China (English)

    刘俊; 梁尚栋

    2011-01-01

    心脏的自主神经包括交感神经与副交感神经.支配心脏的交感神经不仅有传出轴突,也有传递心脏感受的传入神经.心肌缺血可激活心交感传入神经并将信息传递到大脑心血管中枢,通过兴奋交感传出神经引起交感兴奋性反射,出现心率加快和血压升高等现象使心肌缺血、缺氧和心绞痛加重.因此,交感神经功能变化可加重心肌缺血损伤.%The heart autonomic nervous system consists of both sympathetic and parasympathetic nerves. The heart sympathetic nerves contain not only efferent axons, but also the afferentnerve( transmitting messages to the heart ). Myocardial ischemia activates cardiac sympathetic afferent nerve and transmits the information to the brain and cardiovascular centre, which resultsin sympathetic reflex excitability by excitatory sympathetic efferent. This causes an increase in heart rate and blood pressure, leading to the development of myocardial ischemia, hypoxia and angina pain. Therefore, the change in sympathetic function is acontributing factor to myocardial ischemia.

  17. Thematic review series: adipocyte biology. Sympathetic and sensory innervation of white adipose tissue.

    Science.gov (United States)

    Bartness, Timothy J; Song, C K

    2007-08-01

    During our study of the reversal of seasonal obesity in Siberian hamsters, we found an interaction between receptors for the pineal hormone melatonin and the sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT). This ultimately led us and others to conclude that the SNS innervation of WAT is the primary initiator of lipid mobilization in these as well as other animals, including humans. There is strong neurochemical (norepinephrine turnover), neuroanatomical (viral tract tracing), and functional (sympathetic denervation-induced blockade of lipolysis) evidence for the role of the SNS in lipid mobilization. Recent findings suggest the presence of WAT sensory innervation based on strong neuroanatomical (viral tract tracing, immunohistochemical markers of sensory nerves) and suggestive functional (capsaicin sensory denervation-induced WAT growth) evidence, the latter implying a role in conveying adiposity information to the brain. By contrast, parasympathetic nervous system innervation of WAT is characterized by largely negative neuroanatomical evidence (viral tract tracing, immunohistochemical and biochemical markers of parasympathetic nerves). Functional evidence (intraneural stimulation and in situ microdialysis) for the role of the SNS innervation in lipid mobilization in human WAT is convincing, with some controversy regarding the level of sympathetic nerve activity in human obesity.

  18. Estrogen-induced collagen reorientation correlates with sympathetic denervation of the rat myometrium.

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    Martínez, G F; Bianchimano, P; Brauer, M M

    2016-12-01

    Estrogen inhibits the growth and causes the degeneration (pruning) of sympathetic nerves supplying the rat myometrium. Previous cryoculture studies evidenced that substrate-bound signals contribute to diminish the ability of the estrogenized myometrium to support sympathetic nerve growth. Using electron microscopy, here we examined neurite-substrate interactions in myometrial cryocultures, observing that neurites grew associated to collagen fibrils present in the surface of the underlying cryosection. In addition, we assessed quantitatively the effects of estrogen on myometrial collagen organization in situ, using ovariectomized rats treated with estrogen and immature females undergoing puberty. Under low estrogen levels, most collagen fibrils were oriented in parallel to the muscle long axis (83% and 85%, respectively). Following estrogen treatment, 89% of fibrils was oriented perpendicularly to the muscle main axis; while after puberty, 57% of fibrils acquired this orientation. Immunohistochemistry combined with histology revealed that the vast majority of fine sympathetic nerve fibers supplying the myometrium courses within the areas where collagen realignment was observed. Finally, to assess whether depending on their orientation collagen fibrils can promote or inhibit neurite outgrowth, we employed cryocultures, now using as substrate tissue sections of rat-tail tendon. We observed that neurites grew extensively in the direction of the parallel-aligned collagen fibrils in the tendon main axis but were inhibited to grow perpendicularly to this axis. Collectively, these findings support the hypothesis that collagen reorientation may be one of the factors contributing to diminish the neuritogenic capacity of the estrogen-primed myometrial substrate.

  19. The role of the sympathetic nervous system in obesity-related hypertension.

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    da Silva, Alexandre A; do Carmo, Jussara; Dubinion, John; Hall, John E

    2009-06-01

    Obesity is recognized as a major health problem throughout the world. Excess weight is a major cause of increased blood pressure in most patients with essential hypertension and greatly increases the risk for diabetes, cardiovascular diseases, and end-stage renal disease. Although the mechanisms by which obesity raises blood pressure are not completely understood, increased renal sodium reabsorption, impaired pressure natriuresis, and volume expansion appear to play important roles. Several potential mechanisms have been suggested to contribute to altered kidney function and hypertension in obesity, including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, as well as physical compression of the kidneys, especially when visceral obesity is present. Activation of the sympathetic nervous system in obesity may be due, in part, to hyperleptinemia and other factors secreted by adipocytes and the gastrointestinal tract, activation of the central nervous system melanocortin pathway, and baroreceptor dysfunction.

  20. Tension neuropathy of the superficial peroneal nerve: associated conditions and results of release.

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    Johnston, E C; Howell, S J

    1999-09-01

    We reviewed eight patients who sustained superficial peroneal nerve neuralgia after an inversion ankle sprain. Surgical exploration found anatomic abnormalities that tethered the nerve from movement during plantarflexion and inversion of the ankle. Most patients' pain improved dramatically after release and anterior transposition of the nerve. Seven joints also underwent arthroscopy, which showed intra-articular disease that was consistent with the original trauma. Five patients had reflex sympathetic dystrophy, three of which resolved after nerve release. Nerve conduction studies were not helpful. Careful physical examination and local nerve blocks were most important in making the diagnosis and prescribing treatment. All conservative measures should be exhausted before surgery is considered.

  1. Pathology of intracardiac nerves in experimental Chagas disease

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    Ribeiro Lídia Cristina Villela

    2002-01-01

    Full Text Available Severe destruction of intrinsic cardiac nerves has been reported in experimental acute Chagas myocarditis, followed by extensive regeneration during the chronic phase of the infection. To further study this subject, the sympathetic and para-sympathetic intracardiac nerves of mice infected with a virulent Trypanosoma cruzi strain were analyzed, during acute and chronic infection, by means of histological, histochemical, morphometric and electron microscopic techniques. No evidences of destructive changes were apparent. Histochemical demonstration for acetylcholinesterase and catecholamines did not reveal differences in the amount and distribution of intracardiac nerves, in mice with acute and chronic Chagas myocarditis or in non-infected controls. Mild, probably reversible ultrastructural neural changes were occasionally present, especially during acute myocarditis. Intrinsic nerves appeared as the least involved cardiac structure during the course of experimental Chagas disease in mice.

  2. Sympathetic rhythms and cardiovascular oscillations.

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    Montano, N; Cogliati, C; Dias da Silva, V J; Gnecchi-Ruscone, T; Malliani, A

    2001-07-20

    Spectral analysis of heart rate and arterial pressure variabilities is a powerful noninvasive tool, which is increasingly used to infer alterations of cardiovascular autonomic regulation in a variety of physiological and pathophysiological conditions, such as hypertension, myocardial infarction and congestive heart failure. A most important methodological issue to properly interpret the results obtained by the spectral analysis of cardiovascular variability signals is represented by the attribution of neurophysiological correlates to these spectral components. In this regard, recent applications of spectral techniques to the evaluation of the oscillatory properties of sympathetic efferent activity in animals, as well as in humans, offer a new approach to a better understanding of the relationship between cardiovascular oscillations and autonomic regulation.

  3. Sympathetic nervous system activity is associated with obesity-induced subclinical organ damage in young adults.

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    Lambert, Elisabeth; Sari, Carolina Ika; Dawood, Tye; Nguyen, Julie; McGrane, Mariee; Eikelis, Nina; Chopra, Reena; Wong, Chiew; Chatzivlastou, Kanella; Head, Geoff; Straznicky, Nora; Esler, Murray; Schlaich, Markus; Lambert, Gavin

    2010-09-01

    Excess weight is established as a major risk factor for cardiovascular diseases, particularly in young individuals. To get a better understanding of the pathophysiology underlying increased cardiovascular disease risk, we evaluated early signs of organ damage and their possible relationship to sympathetic nervous activity. Eighteen lean (body mass index obese (body mass index >25 kg/m(2)) healthy university students were included in the study. We comprehensively assessed subclinical target organ damage, including the following: (1) assessment of renal function; (2) left ventricular structure and systolic and diastolic function; and (3) endothelial function. Muscle sympathetic nervous activity was assessed by microneurography. Participants with excess weight had decreased endothelial function (Pnervous activity (Pnervous activity (R(2)=0.244; Pnervous activity, after adjustment for body mass index, sex, and blood pressure (R(2)=0.318, P<0.01 and R(2)=0.312, P<0.05, respectively). Excess weight in young individuals is associated with subclinical alterations in renal and endothelial function, as well as in the structure of the heart, even in the absence of hypertension. Sympathetic activity is closely associated with cardiovascular and renal alterations observed in these subjects.

  4. BLOCKADE OF ROSTRAL VENTROLATERAL MEDULLA (RVLM BOMBESIN RECEPTOR TYPE 1 DECREASES BLOOD PRESSURE AND SYMPATHETIC ACTIVITY IN ANESTHETIZED SPONTANEOUSLY HYPERTENSIVE RATS

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    Izabella Silva De Jesus Pinto

    2016-06-01

    Full Text Available IIntrathecal injection of bombesin (BBS promoted hypertensive and sympathoexcitatory effects in normotensive (NT rats. However, the involvement of rostral ventrolateral medulla (RVLM in these responses is still unclear. In the present study, we investigated: (1 the effects of BBS injected bilaterally into RVLM on cardiorespiratory and sympathetic activity in NT and spontaneously hypertensive rats (SHR; (2 the contribution of RVLM bombesin type 1 receptors (BB1 to the maintenance of hypertension in SHR. Urethane-anesthetized rats (1.2 g · kg−1, i.v. were instrumented to record mean arterial pressure (MAP, diaphragm (DIA motor and renal sympathetic nerve activity (RSNA. In NT rats and SHR, BBS (0.3 mM nanoinjected into RVLM increased MAP (33.9 ± 6.6 mmHg and 37.1 ± 4.5 mmHg, respectively; p < 0.05 and RSNA (97.8 ± 12.9 % and 84.5 ± 18.1 %, respectively; p < 0.05. In SHR, BBS also increased DIA burst amplitude (115.3 ± 22.7 %; p < 0.05. BB1 receptors antagonist (BIM-23127; 3 mM