PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Sympathetic Nervous System”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1981

Evidence against an interaction of angiotensin II with the sympathetic nervous system in man.

Animal experiments indicate that angiotensin II can, under some circumstances stimulate the sympathetic nervous system at a number of different sites. In order to determine whether such a relationship of the renin-angiotensin and sympathetic nervous system exists in man, we increased (by intravenous infusion), or decreased (by administering the oral converting enzyme inhibitor captopril) circulating angiotensin II levels and monitored plasma adrenaline and noradrenaline responses. Angiotensin II infusions did not increase plasma catechol-amines, and lowering of angiotensin II by captopril treatment in patients with severe hypertension or congestive heart failure failed to alter plasma adrenaline or nor-adrenaline levels. Whether physiological levels of angiotensin II are capable of interacting directly with the sympathetic nervous system in man remains to be demonstrated.

Adult↗
PubMed1984

The role of the sympathetic nervous system in the cardiovascular effects of systemically administered gamma-aminobutyric acid.

The role of the sympathetic nervous system in the circulatory effects of peripherally administered GABA was investigated in anesthetized dogs. Systemic administration of GABA (10-300 micrograms/kg) decreased blood pressure (BP) by 9-29 mmHg and heart rate (HR) by 15-60 beats/min in anesthetized dogs. Pretreatment with reserpine (1 mg/kg, i.m.) or ganglionic blockade with hexamethonium (10 mg/kg, i.v.) plus atropine (1 mg/kg, i.v.) abolished the GABA-induced hypotension and bradycardia. Intravertebral administration of GABA did not cause greater reduction in BP than by the i.v. route. Bicuculline (1 mg/kg, i.v.) attenuated the BP and HR responses to either intravertebrally or intravenously administered GABA, suggesting peripheral GABA receptors mediate the vasodepressor response to GABA. GABA prevented the bradycardia caused by the preganglionic vagal stimulation, suggesting GABA impairs ganglionic transmission. The depressant effect of GABA on ganglionic transmission was reversed by bicuculline. The depressor and bradycardic effects of i.v. GABA were not mediated by the release of either histamine or prostaglandins, since mepyramine or indomethacin pretreatment failed to alter the BP and HR responses to GABA. Since the doses of GABA used in this investigation probably do not pass the blood brain barrier, it is suggested that systemic administration of GABA decreases BP by a peripheral mechanism that is dependent upon an intact sympathetic nervous system and the ganglionic blocking activity of GABA most likely contributes to its vasodepressor effects upon systemic administration.

Animals↗
PubMed2000

The importance of the sympathetic nervous system and systolic hypertension in patients with hypertension: benefits in treating patients with increased cardiovascular risk.

The sympathetic nervous system is intimately involved in both the origin and the perpetuation of the hypertensive state, although there is some debate as to its precise contribution to the long-term hypertensive condition. Catecholamines are leading candidates to be both the pressor mechanism that initiates the rise in blood pressure and the trophic mechanism that maintains hypertension by vascular hypertrophy. Although the relationship between sympathetic nervous system and systolic blood pressure would seem intuitive, the multiple interactive pathways between these two pathways still needs to be more completely clarified, particularly as relates to interplay with the renin-angiotensin axis. Along this line of reasoning, a number of studies have examined the interplay between ACE inhibitors or angiotensin-receptor antagonists and alterations in sympathetic nervous system activity. Recent data support a role for one of the angiotensin-receptor antagonists, eprosartan, in having a potent inhibitory effect on pre-synaptic type-1 angiotensin receptors (AT(1) -receptors) involved in the enhancement of sympathetic nervous system activity. This may provide an explanation for the differential effect on systolic blood pressure exhibited by this compound.

Antihypertensive Agents↗
PubMed2000

Interaction of carbon dioxide and sympathetic nervous system activity in the regulation of cerebral perfusion in humans.

Recent studies suggest that activation of the sympathetic nervous system either directly or indirectly influences cerebrovascular tone in humans even within the autoregulatory range. In 6 healthy subjects (aged 29+/-4 years), we used transcranial Doppler sonography to determine cerebral blood flow velocity during sympathetic activation elicited through head-up tilt (HUT) and sympathetic deactivation through ganglionic blockade. PaCO(2) was manipulated through hyperventilation and CO(2) breathing (5%). With subjects in the supine position and during HUT, mean arterial pressure was not influenced by PaCO(2). During ganglionic blockade, mean arterial pressure decreased markedly with hyperventilation (-13+/-1.9 mm Hg). Manipulation of sympathetic tone elicited only mild changes in cerebral blood flow (64+/-5.8 cm/s supine, 58+/-4.9 cm/s upright, and 66+/-6.2 cm/s during ganglionic blockade; P:=0.07 by ANOVA). The slope of the regression between PaCO(2) and mean velocity was 1.6+/-0.18 cm/(s. mm Hg) supine, 1.3+/-0.14 cm/(s. mm Hg) during HUT, and 2.3+/-0.36 cm/(s. mm Hg) during ganglionic blockade (P:<0.05). Spontaneous PaCO(2) and ventilatory response to hypercapnia were also modulated by the level of sympathetic activity. Changes in sympathetic tone have a limited effect on cerebral blood flow at normal PaCO(2) levels. However, the sympathetic nervous system seems to attenuate the CO(2)-induced increase in cerebral blood flow. This phenomenon may indicate a moderate direct effect of the sympathetic nervous system on the cerebral vasculature. Furthermore, sympathetic activation tends to increase ventilation and thus can indirectly increase cerebrovascular tone.

Adult↗
PubMed1988

Effect of experimental hyperinsulinemia on sympathetic nervous system activity in the rat.

Since insulin acutely stimulates the sympathetic nervous system, a role for sympathetic overactivity has been hypothesized to underlie the association between chronic hyperinsulinemia and hypertension. To assess the effect of sustained hyperinsulinemia on sympathetic function, [3H]norepinephrine (NE) turnover was measured in rats injected with insulin for 14d. NE turnover in insulin-treated animals given free access to lab chow and a 10% sucrose solution was compared with that obtained in rats fed chow alone or chow plus sucrose. Sucrose ingestion increased NE turnover in heart, brown adipose tissue, and liver, but exogenous insulin did not augment turnover beyond that seen in animals given sucrose alone. This study, therefore, provides no evidence that chronic hyperinsulinemia, sufficient to induce peripheral insulin resistance, stimulates sympathetic activity more than that produced by chronic sucrose ingestion.

Adipose Tissue, Brown↗
PubMed1994

Vascular angiotensin and the sympathetic nervous system: do they interact?

We tested the hypothesis that local vascular formation of angiotensin (ANG) II and the sympathetic nervous system potentiate each other. Isolated rat hindquarters were perfused with an artificial medium, and ANG I and II release was measured by high-performance liquid chromatography and radioimmunoassay. Electrical stimulation of the lumbar sympathetic chain (0.5, 2, and 8 Hz) did not affect vascular ANG release in Sprague-Dawley (SD) rats. Hypertensive, ren-2 transgenic (TG+) rat hindquarters released significantly more ANG I (110 +/- 19 vs. 65 +/- 21 fmol/30 min in SD rats) and ANG II (235 +/- 22 vs. 140 +/- 30 fmol/30 min); however, nerve stimulation did not alter ANG release in TG+ rats. Captopril inhibited vascular ANG II release by 90%, but neither captopril nor ANG II receptor blockade by losartan affected the pressor response to nerve stimulation in SD and TG+ rats. Isoproterenol failed to increase either vascular ANG release or pressor response to nerve stimulation in SD or spontaneously hypertensive rat hindquarters. Exogenous renin, which increased vascular ANG release approximately 100-fold, prolonged the pressor responses to nerve stimulation. We conclude that the vascular renin-ANG system does not interact with the sympathetic nervous system locally. However, high concentrations of ANG II, which can be induced by circulation-derived renin, may prolong the duration of sympathetic nerve-induced vasoconstriction.

Adrenergic beta-Agonists↗
PubMed1992

Hypertension in blacks: socioeconomic stress and sympathetic nervous system activity.

Primary hypertension is almost twice as prevalent among American blacks as among whites. Causes of this increased prevalence of hypertension remain elusive. Elevation of sympathetic nervous system activity, in part secondary to increased levels of socioeconomic stress, is hypothesized as playing a role. Increased sympathetic nervous system activity may increase peripheral vascular resistance directly or through increased vascular reactivity. Microneurography allows direct measurement of peripheral sympathetic nervous system activity. Application of this technique will allow comparison of sympathetic nervous system activity in black and white subjects and provide additional insight into the role of the sympathetic nervous system in the development of hypertension in blacks.

Black or African American↗
PubMed2000

Scintigraphic assessment of regional cardiac sympathetic nervous system in patients with single-vessel coronary artery disease.

In coronary artery disease, the cardiac sympathetic nervous system is closely associated with myocardial ischemia. I-123 metaiodobenzylguanidine (MIBG) imaging allows us to assess the cardiac sympathetic nervous system regionally. One-hundred and eleven patients with single-vessel disease underwent regional quantitative analysis of MIBG imaging before successful percutaneous transluminal coronary angioplasty (PTCA), and repeat angiography 6 months after PTCA. Based on the results of the follow-up left ventriculogram, patients were divided into 3 groups: 39 angina pectoris (AP), 48 prior myocardial infarction without asynergy (MI without asynergy) and 24 prior myocardial infarction with asynergy (MI with asynergy). AP and MI without asynergy had significant correlations between uptake parameters and regional washout in the territory of diseased vessels, among which the severity score in AP was the most closely correlated with regional washout (r = 0.79, p < 0.0001). These correlations disappeared in MI with asynergy. To compare regional MIBG parameters in the territory of the diseased vessel as well as in the territories of the other major coronary arteries among the 3 groups, we examined MIBG parameters in 57 patients with left anterior descending artery (LAD) disease selected from among the study patients. Regional washout in the territory of the LAD was significantly higher in the MI without asynergy group than in the other two groups. The left circumflex artery (LCX) region showed significantly reduced MIBG uptake and an increased extent score in the MI with asynergy group compared with the AP group, although only a difference in the extent score existed between the MI with asynergy group and the AP group in the right coronary artery (RCA) region. In addition, the global ejection fraction before PTCA showed a significant negative correlation with each regional washout rate. In this way, regional quantitative analysis of MIBG imaging can detect the regional differences in the cardiac sympathetic nervous system in coronary artery disease, which may be associated with the degree of regional left ventricular dysfunction due to myocardial ischemia.

3-Iodobenzylguanidine↗
PubMed1989

The contribution of the sympathetic nervous system to hypertension in diabetes mellitus.

Hyperactivity of the sympathetic nervous system has repeatedly been assumed to play a role in the pathogenesis of essential hypertension. Particularly in young hypertensive patients, sympathetic nervous activity seems to be slightly elevated. On the other hand an increased pressor effect of noradrenaline has also been reported in some patients with essential hypertension. While neither the slightly elevated sympathetic tone nor the inconstant increased reactivity to noradrenaline could alone be responsible for the blood pressure elevation, both factors together appear to form an important determinant of the level of arterial blood pressure. There is no uniform evidence that sympathetic nervous activity is changed in uncomplicated diabetes. A diminished sympathetic nervous activity in patients with secondary complications is so far not proved. A slight increase in circulatory reactivity to noradrenaline is described independent of the height of blood pressure, however, data in moderate and accelerated hypertensive diabetic patients are not available.

Diabetes Complications↗
PubMed1987

Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate-salt hypertensive rats.

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA-salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.

Analysis of Variance↗