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At least 487 records · Page 27Linked to original sources
PubMed1987

Vagal cold block in area postrema-lesioned dogs: interaction of vasopressin and sympathetic nervous system.

This study evaluated the interaction between arginine vasopressin (AVP) and the sympathetic nervous system (SNS) during bilateral vagal cold block (BVB) and the arterial baroreflex response to phenylephrine (PE) and exogenous AVP in conscious sham-operated (sham) and area postrema (AP)-lesioned mongrel dogs. The hemodynamic responses to ganglionic blockade (GB) and the vascular (V1) AVP receptor antagonist [d(CH2)5Tyr(Me)]AVP (AVPX) were similar in sham and AP-lesioned dogs. Elimination of the AVP pressor system by AVPX in sham dogs did not alter the pressor response to BVB, whereas subsequent blockade of the SNS by GB abolished the response to BVB. When GB was first imposed, however, it alone eliminated only 55% of the pressor response to BVB, whereas subsequent AVPX eliminated the remaining pressor response to BVB. In contrast, in AP-lesioned dogs, AVPX alone substantially reduced the pressor response to BVB. Additionally, the apparent contribution of each pressor system to the response to BVB was not enhanced in the absence of the other system, as had been seen in the sham dogs. These data indicate that during interruption of vagal afferent activity, reflexly released AVP appears to limit the reflex activation of the SNS. This interaction of AVP with the cardiopulmonary reflex is eliminated following ablation of the area postrema. Infusion studies with PE and AVP indicate that AVP significantly augments baroreflex inhibition of heart rate when compared with PE. Ablation of the area postrema did not alter the arterial pressure-heart rate relationship obtained with PE but eliminated the augmented response to AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Effect of long-term beta-blocker therapy on microvolt-level T-wave alternans in association with the improvement of the cardiac sympathetic nervous system and systolic function in patients with non-ischemic heart disease.

The purpose of this study was to test a hypothesis that T-wave alternans (TWA) is improved in association with an improvement in cardiac sympathetic nervous system and systolic function by oral beta-blocker therapy in patients with non-ischemic heart disease (NIHD). TWA testing, (123)I-metaiodobenzylguanidine (MIBG) imaging and echocardiography were performed at the baseline and 3 months after beta-blocker therapy in 26 patients with NIHD and positive TWA. The alternans voltage (V(alt)), the heart-to mediastinal-ratio on the early (e-H/M) and delayed (d-H/M) images, the washout rate (WR), the left ventricular ejection fraction (LVEF), and the calculated rate of change by beta-blocker therapy in each parameter (ie, deltaV(alt), deltae-H/M, deltad-H/M, deltaWR and deltaLVEF) were measured. After therapy, TWA turned negative in 8 patients (group A) and remained positive in 18 (group B); V(alt) was significantly decreased in group B (p<0.001). In group A, e-H/M, d-H/M and LVEF were significantly increased (e-H/M: p<0.05, d-H/M and LVEF: p<0.01), as were e-H/M and LVEF in group B (p<0.05). There were significant correlations between deltaV(alt) and deltae-H/M (r=-0.61, p<0.01), deltad-H/M (r=-0.82, p<0.0001), deltaWR (r=0.60, p<0.01) and deltaLVEF (r=-0.70, p<0.01). In patients with NIHD, the TWA is improved in association with the improvement in cardiac sympathetic nervous system abnormalities and left ventricular systolic dysfunction by beta-blocker therapy.

Action Potentials↗
PubMed1998

Role of the sympathetic nervous system in human hypertension.

Animal studies have shown conclusively that sympathetic neural factors are involved in the development and/or maintenance of high blood pressure. Whether this is also the case for human hypertension has been documented less conclusively, owing to technical difficulties in assessing human adrenergic function. Recent studies have used sophisticated and sensitive techniques to evaluate sympathetic activity in humans, e.g. the norepinephrine spillover method and the microneurographic quantification of sympathetic nerve traffic, allowing documentation of the participation of adrenergic mechanisms in the early and late phases of the hypertensive process. Evidence has been also provided that the activation of the sympathetic nervous system (1) is peculiar to the essential hypertensive state, (2) parallels the degree of the blood pressure elevation, (3) is triggered by reflex and humoral mechanisms and (4) may exert deleterious metabolic and cardiovascular effects, accelerating the progression of the end organ damage accompanying hypertension. These findings explain why non-pharmacological and pharmacological approaches to the treatment of hypertension should be aimed not only at lowering elevated blood pressure values but also at exerting sympathoinhibitory effects.

Animals↗
PubMed1987

Role of sympathetic nervous system in hypotensive action of taurine in DOCA-salt rats.

We tested the hypothesis that the antihypertensive effects of dietary taurine supplementation in deoxycorticosterone acetate (DOCA)-salt rats may be attributed to the suppression of sympathetic nervous system activity. In uninephrectomized rats treated with DOCA while receiving 1% NaCl solution for 2 weeks, systolic blood pressure was significantly increased as compared with that in control rats treated with vehicle suspension and tap water. Sympathetic nervous system activity was assessed by tissue norepinephrine turnover, which was determined from the rate of decline of tissue norepinephrine concentration after the administration of alpha-methyl-p-tyrosine, a potent inhibitor of the rate-limiting step of catecholamine synthesis. Cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure (4 degrees C, 8 hours) were markedly increased in DOCA-salt rats as compared with control rats. Also, DOCA-salt rats had increased depressor response to hexamethonium bromide, a ganglion blocker. In contrast, supplementation of 1% taurine in DOCA-salt rats attenuated the development of the hypertension associated with the normalization of both the increased depressor response to ganglionic blockade and the accelerated cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure. Taurine supplementation in control rats, however, had no effect on blood pressure or norepinephrine turnover during cold exposure. These results suggest that taurine supplementation suppresses sympathetic overactivity in DOCA-salt rats, thus leading to inhibition of the development of hypertension.

Animals↗
PubMed1985

Relationship of sodium sensitivity and the sympathetic nervous system.

To test the hypothesis that salt-sensitive hypertension reflects an abnormal response of the sympathetic nervous system (SNS) to salt, arterial pressure and plasma norepinephrine (NE) concentration were measured in 23 black hypertensive patients and 28 black normotensive control subjects during 4 days of salt depletion and 3 days of salt loading. When the sequence was salt depletion followed by salt loading, plasma NE rose with salt depletion and was suppressed by salt loading. In normotensive subjects, plasma NE with salt loading returned to control values, but in hypertensive patients it remained elevated suggesting SNS stimulation by the salt load. Plasma NE responses of hypertensive patients did not distinguish between those who became normotensive with salt depletion from those who did not. The sequence was reversed with salt loading preceding salt depletion, to investigate further these abnormal plasma NE responses to salt loading. With this sequence, plasma NE was only slightly and insignificantly reduced by salt loading and responses of hypertensive patients were similar to those of normotensive subjects. In contrast, plasma NE rose with salt depletion as before. With both protocols plasma NE correlated inversely with urinary sodium excretion as previously described. These results in black hypertensive patients are not consonant with those obtained in other studies of primarily white hypertensive patients, suggesting that salt-sensitive hypertension may have a different mechanism in blacks than in whites.

Black People↗
PubMedDate not supplied

Relation of sodium-potassium adenosine triphosphatase inhibitor to sympathetic nervous system during salt-loading in essential hypertension.

The present study was designed to assess if the release of Na-K ATPase inhibitor (NKAI) after salt-loading is related to sympathetic nervous system in essential hypertension. Thirteen patients with essential hypertension were studied during low-salt diet (2 g/day) and then high-salt diet (20 g/day) for each 7-days period. Mean blood pressure (MBP), body weight, Na:K ratio in red blood cell (R-Na/K), plasma norepinephrine (PNE) and NKAI were measured on the last day of each period. NKAI was determined by the degree of the inhibition of dog kidney Na-K ATPase activity by deproteinized plasma. Patients were classified as "salt-sensitive" (SS) or "nonsalt-sensitive" (NSS) group by the MBP responses to salt-loading. With the high-salt diet, SS group showed more body weight gain, greater increase in R-Na/K and NKAI (SS; 8.0 +/- 1.0%, NSS; 2.4 +/- 0.8%, P less than 0.01) than NSS group. PNE showed no changes in SS group and decreased in NSS group (P less than 0.05). The increase of MBP was highly correlated with the rise of NKAI (r = 0.76, P less than 0.01). Moreover, the increase of NKAI was also significantly correlated with the changes of PNE (r = 0.62, P less than 0.05). These results suggest that the greater increase in blood pressure by salt-loading in SS patients can be attributed to the increase of NKAI, which might regulate the sympathetic nervous system as a result of increased intracellular sodium.

Adult↗
PubMed1993

[Individual differences in sympathetic nervous system responses to white noise stimuli: an investigation by finger plethysmogram].

Possible individual variations in the sympathetic nervous system response to sound stimuli were investigated using the auditory evoked plethysmogram response (AEPGR). This study consists of the following 3 experiments; (EXP1) the sound level-response relationships between white noise at 50, 70, and 90 dB (A) and AEPGRmax as defined below, (EXP2) individual variations of AEPGRmax to white noise at 90 dB (A), and (EXP3) the relationship between the AEPGR pattern and the urinary catecholamine (CA) excretion rate during sleep on the preceding night. The subjects were 35 young persons in (EXP1), and 79 young (18-28 yrs. old) and 35 old (60-83 yrs. old) persons in (EXP2) and (EXP3), respectively. The results were: (1) a good sound level-response relationship between the sound levels of 50, 70, and 90 dB (A) and AEPGRmax was obtained on average; (2) an AEPGRmax of more than 100% in response to the 90 dB (A) white noise was found in about 10% of the subjects, whereas it was below 100% in 90% of them. The time prior to the maximum response in the former case varied from 4.6 to 22.2 sec, which was quite a contrast to that of 3.0-9.0 sec in the latter case; (3) The NE (norepinephrine), E (epinephrine) and DA (dopamine) excretion rates were shown to be significantly higher in the former group in (2) than in the other groups, regardless of adjustment for age, blood pressure and/or ECG findings. Thus, it is suggested that the cardiac response to E secreted from the adrenals due to white noise stimuli was predominant in the former group in (2). Therefore, this response pattern was called the AEPGR "beta type", whereas the other group was designated the "alpha type", since its AEPGR appeared to reflect only vasoconstriction. The suggested individual differences in AEPGR associated with increased night-rest catecholamine secretion were also discussed in relation to their possible relevance to chronic stress, neuroticism and other conditions.

Adolescent↗
PubMedDate not supplied

Pathogenesis of hypertension in renal failure: role of the sympathetic nervous system and renal afferents.

1. The kidney receives a dense innervation of sympathetic and sensory fibres and can be both a target of sympathetic activity and a source of signals that drive sympathetic tone. In the normal state, interactions between the kidney and sympathetic nervous system (SNS) serve to maintain blood pressure and glomerular filtration rate within tightly controlled levels. In renal failure, a defect in renal sodium excretory function leads to an abnormal pressure natriuresis relationship and activation of the renin-angiotensin-aldosterone system, contributing to the development of hypertension and progression of kidney disease. 2. Evidence now strongly indicates a role for the SNS in the pathogenesis of hypertension in renal failure. Hypertension occurs commonly and early in renal disease and is paralleled by increases in SNS activity, as indicated by increased muscle sympathetic nerve activity and circulating catecholamines. This appears to be driven by the diseased kidneys, because nephrectomy or denervation has been shown to correct blood pressure and SNS activity in human and animal studies. 3. Afferent signals from the kidney, detected by chemoreceptors and mechanoreceptors, feed directly into central nuclei of the SNS, including the hypothalamus and circumventricular organs, in addition to the stimulus provided by circulating and brain-derived angiotensin II. Therefore, the pathogenesis of hypertension in renal failure is complex and arises from the interaction of haemodynamic and neuroendocrine factors. 4. Increased SNS activity has significant implications with regard to increased risk of cardiovascular disease and is an important consideration in the treatment of renal failure.

Afferent Pathways↗
PubMedDate not supplied

Carvedilol improves left ventricular function in heart failure patients with idiopathic dilated cardiomyopathy and a wide range of sympathetic nervous system function as measured by iodine 123 metaiodobenzylguanidine.

BACKGROUND: Carvedilol treatment reduces the mortality rate in patients with congestive heart failure. It is not known whether carvedilol treatment is effective in heart failure patients with substantial cardiac sympathetic nerve dysfunction. The goal of this study was to determine the effect of chronic carvedilol treatment in patients with cardiac sympathetic nerve dysfunction of varying severity. METHODS AND RESULTS: In 22 congestive heart failure patients with idiopathic cardiomyopathy, sympathetic nerve function was assessed before and after 7.2 +/- 2.7 months of carvedilol treatment with the use of iodine 123 metaiodobenzylguanidine (MIBG) imaging, radionuclide ventriculography, and transmyocardial norepinephrine sampling. Patients with relatively advanced impairment of cardiac sympathetic nerve function, as manifested by a baseline I-123 MIBG ratio lower than 1.40, had a statistically significant improvement in I-123 heart-mediastinum ratio with carvedilol treatment, from 1.26 +/- 0.12 to 1.39 +/- 0.20 (P =.004). Of 10 patients with a baseline I-123 MIBG ratio lower than 1.40, 9 had an increase in the heart-mediastinum ratio with carvedilol treatment. Left ventricular ejection fraction increased from 25.4% +/- 7.8% to 37.3% +/- 14.7% (P <.001), with no difference between patients with relatively advanced versus relatively preserved cardiac sympathetic nerve function. CONCLUSION: Most patients with congestive heart failure show a favorable response in left ventricular function to carvedilol treatment, regardless of the baseline level of cardiac sympathetic nervous system function, as assessed by neuronal imaging with I-123 MIBG. Patients with relatively advanced impairment of baseline I-123 MIBG uptake are most likely to show evidence of improved cardiac sympathetic nervous system function in response to carvedilol therapy.

3-Iodobenzylguanidine↗
PubMed1989

Results of the multicenter antihypertensive treatment trials. Therapeutic implications and the role of the sympathetic nervous system.

The results of 19 antihypertensive treatment trials spanning some 20 years of research showed that treatment had significant benefits for pressure-related complications of hypertension but generally did not prevent coronary artery disease morbidity or mortality. As possible reasons for this relative failure were explored, new emphasis was placed on the role of the sympathetic nervous system in the vascular complications of hypertension. Most risk factors for coronary artery disease strongly involve the sympathetic nervous system, which may be the final common pathway for their adverse effects. The antihypertensive drugs used in most of the large clinical trials were associated with enhanced sympathetic activity. Moreover, excessive sodium depletion caused by large doses of diuretics and dietary low-sodium intake may have contributed to the treatment's ineffectiveness in preventing primary coronary disease. The implications of the research for antihypertensive treatment are discussed, with an emphasis on the physiologically appropriate role of clonidine therapy.

Antihypertensive Agents↗
PubMed1972

The role of the sympathetic nervous system in hypoglycaemia-stimulated gastric secretion.

The gastric secretory response to insulin is mediated predominantly by the vagus. The associated hypoglycaemia stress response is mediated by the sympathetic nervous system. Inhibition of the sympathetic response by simultaneous alpha and beta receptor blockade was studied in five healthy young adults. No appreciable modification of gastric secretory output resulted.

Adrenocorticotropic Hormone↗
PubMed2001

Sympathetic nervous system activity in adipose tissues during pregnancy and lactation of the rat.

The concentration and turnover of norepinephrine in white adipose and liver tissues were determined in pregnant, lactating, and age-matched virgin rats to elucidate the adaptations in sympathetic nervous system activity. In study 1, at d 18 of pregnancy and d 7 and 21 of lactation, animals were killed, and liver and cardiac perimetrial and retroperitoneal adipose depots were quick-frozen and then assayed for norepinephrine as a gross estimate of sympathetic innervation. In study 2, the same design was used to measure the turnover of norepinephrine as a measure of sympathetic activity. Animals were treated with alpha-methylparatyrosine, an inhibitor of norepinephrine synthesis, and killed at 0, 1.5, and 3 h after injection. In pregnant animals, basal norepinephrine concentrations were decreased compared with unbred controls in perimetrial and retroperitoneal depots. By d 21 of lactation, all adipose depots from lactating animals had more norepinephrine than did controls. The turnover of norepinephrine decreased in noncardiac adipose depots of pregnant animals. By d 21 of lactation, norepinephrine concentration was greater in all of the adipose depots than in controls. The turnover rate was faster in all adipose tissue depots but only significantly different in the cardiac depot. Sympathetic nervous activity in adipose tissue is diminished in pregnant rats, presumably to save energy for fetal growth and maternal fat storage. In late lactation, activity is increased, presumably to direct fatty acids away from adipose tissue towards milk production. The data from this study are consistent with the hypothesis that the sympathetic nervous system plays a role in the regulation of adipose metabolism in lactation.

Adaptation, Physiological↗
PubMed1984

Sympathetic nervous system and exercise tolerance response in normotensive and hypertensive adolescents.

Comparative evaluation of isometric and dynamic exercise performance in normotensive, borderline hypertensive and hypertensive adolescents was made. Hemodynamic changes were correlated with level of adrenergic sympathetic nervous system activity as measured by plasma epinephrine and norepinephrine values. No significant intergroup differences were found with respect to isometric exercise with the exception of high peak isometric exercise heart rates and plasma epinephrine levels in the patients with significant hypertension. During dynamic treadmill testing, patients with the most marked hypertension demonstrated a statistically significantly greater tachycardia response to exercise that correlated with highest peak exercise epinephrine levels. The most hypertensive systolic dynamic exercise response was evidenced in the borderline hypertensive group in which peak exercise norepinephrine values were significantly higher than in other groups. Maximal exercise serum lactate levels were higher in hypertensive patient groups than in normotensive subjects. Altered hemodynamic response to peak dynamic exercise appears to exist in adolescents with borderline and significant hypertension and is in part mediated by altered activity of the sympathetic nervous system.

Adolescent↗
PubMed1991

[Role of sympathetic nervous system on blood pressure and heart rate variabilities in the rat: spectral analysis].

The role of the sympathetic nervous system (SNS) in the genesis of the beat-to-beat variability of blood pressure (BP) and heart rate (HR) was studied using spectral analysis. The SNS activity of genetically normotensive rats of the Lyon strain (LN) was abolished in 2 ways: 1) adrenergic blockade with administrations of phentolamine (PHE, 5 mg/kg i.v.) or propranolol (PRO, 5 mg/kg i.v.) or both drugs (PHEPRO) or 2) destruction of the sympathetic fibers with an early chronic treatment with guanethidine (LNSx). HR and systolic (SBP) and diastolic (DBP) BP spectra were computed using 50 to 100 stationary sequences from 1 h beat-to-beat recordings and covered the 0.015-3.85 Hz frequency band. In LN rats, spectra obtained in baseline conditions exhibited a high-frequency peak (HF, 1.04-1.13 Hz) related to the respiratory frequency and a mid-frequency peak (MF, 0.38-0.45 Hz). Concerning BP, the alterations of the SNS induced significant decreases of the total modulus (mmHg/Hz1/2) of the MF band (0.27-0.74 Hz): [formula: see text] In addition, the MF peak of SBP and DBP spectra was abolished in LNSx and PHEPRO rats. Concerning HR spectra, the moduli of all the frequency components were decreased in PHEPRO rats only. In conclusion, the similarity of the results observed in LNSx and PHEPRO rats shows that the MF oscillations of BP depend in a large extent (65%) on the action of the sympathetic fibers and involve the activation of both alpha- and beta-adrenoceptors. Concerning DBP, this effect is especially mediated by the activation of alpha-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of physiological and pharmacological variation of sympathetic nervous system activity on plasma non-esterified fatty acid concentrations in man.

1. The consequence of the sympatholytic effect of clonidine (alpha 2-adrenoceptor agonist) was compared with the effect of a physiological inhibition of sympathetic nervous system activity (change from upright to supine position) on plasma catecholamine and non-esterified fatty acid (NEFA) concentrations in overnight fasting healthy men. 2. Clonidine (150 micrograms orally) administered in upright position induced a significant reduction of plasma noradrenaline and NEFA concentrations. A change from upright to supine position which provoked a more marked decrease in plasma noradrenaline concentrations induced a weak increase in plasma NEFA concentrations. 3. The modification of plasma NEFA and catecholamine concentrations brought about by standing up was studied after placebo or yohimbine (alpha 2-adrenoceptor antagonist) administration. With placebo, standing up promotes a 100% increase in plasma noradrenaline concentrations (measured 5 and 15 min after rising) and a weak transient decrease in plasma NEFA concentrations (5 min after rising). In the supine position, yohimbine increased plasma noradrenaline and NEFA concentrations by about 100% and 55% respectively. Standing after yohimbine administration promoted large increases in plasma noradrenaline and NEFA concentrations. 4. These results indicate that a reduction of sympathetic nervous activity is not associated with a decrease of plasma NEFA concentrations and argue for a role of alpha 2-adrenoceptors in the NEFA mobilization from adipose tissue after sympathetic nervous system activation in man.

Adult↗