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 577 records · Page 32Linked to original sources
PubMed1989

Salt sensitivity in human essential hypertension: effect of renin-angiotensin and sympathetic nervous system blockade.

We studied the acute effect of oral captopril (25mg) and clonidine(300 micrograms) on blood pressure (BP) in patients with essential hypertension successively maintained on a low (LSD) and high (HSD) salt diet. Seven patients were salt sensitive (SS) and seven were salt resistant (SR). The maximal decrease in diastolic BP caused by captopril in patients on the LSD was greater in SS than SR individuals. Baseline urinary norepinephrine levels did not change from LSD to HSD (p greater than 0.05) in SS patients and decreased in SR patients (p less than 0.05). The maximal decrease in mean BP during the clonidine test was the same for both diets (p greater than 0.05) in SS patients and was lower (p less than 0.05) for the HSD in SR patients. SS patients on the HSD presented a higher decrease in systolic BP than SR patients (p less than 0.05) during the clonidine test. These data suggest overactivity of the renin-angiotensin system in SS patients on the LSD and of the sympathetic nervous system in SS patients on the HSD and that the clonidine test could be a good indicator for identifying SS and SR patients.

Adult↗
PubMed1996

[Reduced sympathetic nervous system activity during the cluster period of cluster-headache].

Cluster headache is a rare, very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. Alterations of the hypothalamic-pituitary axis due to chronobiological changes, such as typical temporal pattern of both cluster periods and attacks, point to a central etiopathogenesis. Multiple local and systemic autonomic symptoms are compatible with an altered balance of the sympathetic and parasympathetic nervous system. In this connection, too, a central etiology is postulated. To evaluate the activation of the sympathetic nervous system, in 12 cluster headache patients we investigated the plasma catecholamines norepinephrine and epinephrine four times a day (7.00, 12.00, 17.00, 23.00) in the cluster period. In the cerebrospinal fluid we determined the transmitters norepinephrine, epinephrine, dopamine and the metabolites homovanillic acid (HVA), vanillymandelic acid (VMA) and 5-hydroxyindoleacetic acid (5-HIAA). Values of plasma norepinephrine in the morning (p < 0.01), in the evening (p < 0.01) and the daily mean value (223.8 = 58.3 nmol/ml) were significantly decreased in the cluster headache group in comparison to the control group (328.8 = 53.0 nmol/ml, p < 0.01). The plasma epinephrine showed no significant changes. In the CSF of cluster headache patients norepinephrine (p < 0.05), HVA (p < 0.01), and 5-HIAA (p < 0.01) were significantly decreased. Plasma norepinephrine was correlated with CSF values of HVA and 5-HIAA. The longer the duration of the disease, the lower the values of HVA and 5-HIAA in the CSF of cluster headache patients. Moreover, plasma norepinephrine showed a significant correlation with the duration, the intensity and the frequency of the attacks. The results of this study implicate decreased activity of the sympathetic nervous system with alteration of circadian rhythmicity during the cluster period. The decreased CSF transmitter values may support the hypothesis of a central etiopathogenesis of cluster headache. Moreover, plasma norepinephrine seems to be involved in triggering and continuing the attacks. The anatomical region in which this interface of sympathetic and neurogenic inflammatory processes might be located is the trigemino-vascular system.

Adult↗
PubMed1992

Effect of low-calorie diets on the sympathetic nervous system, body weight, and plasma insulin in overweight hypertension.

When weight reduction was found to decrease blood pressure in the overweight hypertensive patient, it was hailed as the causative factor. A growing number of recent studies indicate that this association may be secondary to a correlation between diet-associated metabolic change and the sympathetic nervous system. A select group such as overweight hypertensive patients may have a genetic predisposition for such a correlation. In overweight hypertensive patients, low-calorie diet and especially very-low-calorie diet, correlate with improved glucose metabolism, a decrease in plasma insulin concentration, and altered norepinephrine concentrations and thus sympathetic nervous system activity. Several of these studies also show a lack of effect of salt intake on blood pressure. Thus, it seems that metabolic changes caused by the decrease in caloric intake are responsible for the decrease in blood pressure. These must be investigated to understand the effect of the different diets on blood pressure. Very low-calorie diets were found very useful in breaking the vicious circle of severe nonresponsive hypertension to medication.

Blood Pressure↗
PubMedDate not supplied

Sodium sensitivity and sympathetic nervous system in hypertension induced by long-term nitric oxide blockade in rats.

1. Pharmacological inhibition of nitric oxide (NO) synthesis is known to produce acute and chronic hypertension in many animal species, but the underlying mechanisms mediating the hypertension are not completely understood. In particular, the pathogenetic roles of sodium sensitivity and the sympathetic nervous system in this model of hypertension are controversial. The present study was designed to test the hypothesis that long-term administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) to male Sprague-Dawley rats would produce a sodium-sensitive hypertension and that the enhanced activity of the sympathetic nervous system in this type of hypertension contributes to the sodium sensitivity. 2. NG-Nitro-L-arginine methyl ester was added to drinking fluid for 8 weeks at a concentration of 16 mg/dL. Rats received tap water for the first 4 weeks of the study and were then divided into two groups and placed on either a normal or high sodium intake (ingestion of either tap water or 0.9% NaCl, respectively). Awake systolic blood pressure was measured by the tail-cuff method every week. Urinary excretion rates of the stable NO metabolites and catecholamines during NO synthesis inhibition were examined. 3. Long-term administration of L-NAME produced a marked and sustained elevation in arterial pressure without altering urine flow, or sodium excretion rate. NG-Nitro-L-arginine methyl ester-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites NO2- and NO3- and was aggravated when rats drank 0.9% NaCl in place of tap water. Urinary excretion of adrenaline and noradrenaline, but not dopamine, in L-NAME-treated rats increased significantly within the first week of the study compared with control rats. L-Arginine (2 g/dL in drinking fluid) completely reversed the elevation of arterial pressure as well as the decrease in urinary NO2- and NO3- excretion and the increased urinary excretion of catecholamines associated with L-NAME treatment by 3 weeks of concomitant administration. 4. These results suggest that long-term inhibition of NO synthesis produces a sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension.

Animals↗
PubMed1990

Effect of regional myocardial ischemia on sympathetic nervous system as assessed by fluorine-18-metaraminol.

With the introduction of radiolabeled catecholamine analogues, the noninvasive evaluation of the cardiac sympathetic nervous system has become possible. This study evaluated the effect of regional ischemia on myocardial retention of the new norepinephrine analogue 6-[18F] fluorometaraminol (FMR) in the open chest dog model. Six dogs were injected intravenously with FMR following 30-min occlusion of the left anterior descending artery. Six sham animals served as control group. Regional myocardial blood flow as determined by microspheres decreased 87% during ischemia (p less than 0.01), but was not significantly different from control myocardium following reperfusion. Regional myocardial 18F activity as determined postmortem was significantly reduced in reperfused myocardium (-34%), which paralleled an 18% reduction of tissue norepinephrine concentration. Thus, short time periods of coronary occlusion affect neuronal function indicating the sensitivity of the sympathetic nerve terminals to ischemia. FMR provides a new tracer approach for the characterization of neuronal integrity in postischemic myocardium.

Animals↗
PubMedDate not supplied

Vascular and humoral sympathetic nervous system reactivity during mental arithmetic in primary Raynaud's phenomenon.

To investigate the hypothesis of a sympathetic imbalance in the pathophysiology of digital vasospasms during stress we measured vascular and sympathetic nervous system reactivity during a standardized mental arithmetic test in 12 patients with primary Raynaud's phenomenon in comparison to 12 healthy control subjects. Blood pressure, heart rate, forearm blood flow and fingertip laser Doppler flux were measured together with the venous concentrations of norepinephrine and epinephrine from the back of the hand before and during mental arithmetic in a climate room. No significant differences in circulatory or sympathetic reactivity were found between both groups except for fingertip skin circulation with a small decrease of laser Doppler flux (-11.6%) in controls, whereas it increased in PRP (46.6%; p less than 0.05 between both groups). Baseline skin blood flow was inversely correlated with changes in laser Doppler flux (R = -0.91; p less than 0.001; no. 24) irrespective of the diagnosis when baseline skin bloodflow is low a vasodilatory response occurs and when it is high a vasoconstrictive response is seen. Initial laser Doppler flux was lower while baseline diastolic blood pressure, heart rate and (nor)epinephrine concentrations were significantly higher in Raynaud-patients suggesting an increased sympathetic activity at rest in primary Raynaud's phenomenon.

Adult↗
PubMed1999

Effects of amlodipine and cilnidipine on cardiac sympathetic nervous system and neurohormonal status in essential hypertension.

N-Type calcium channel antagonists may suppress sympathetic activity. The purpose of this study was to assess the effects of amlodipine and cilnidipine on the cardiac sympathetic nervous system and the neurohormonal status of essential hypertension. 123I-metaiodobenzylguanidine (MIBG) cardiac imaging was performed and blood samples were taken to determine plasma renin activity and plasma norepinephrine concentration before and 3 months after drug administration in 47 patients with mild essential hypertension. Twenty-four of the patients were treated with 5 to 10 mg/d of amlodipine; the other 23 were treated with 10 to 20 mg/d of cilnidipine. For comparison, 12 normotensive subjects were also studied. No significant differences were found in the basal characteristics between the 2 hypertensive groups. In both hypertensive groups, both the systolic and diastolic blood pressures were significantly reduced to similar levels 3 months after drug treatment. Before the drug treatment, the 2 hypertensive groups had a significantly higher washout rate and lower heart-to-mediastinum (H/M) ratio compared with the normotensive subjects. The H/M ratio significantly increased (P<0.05) in combination with a decreased washout rate (P<0.02) after drug treatment in the cilnidipine group. In the amlodipine group, a significant decrease in washout rate (P<0. 04) was noted, without an increase in the H/M ratio. However, no significant changes were found in plasma renin activity and plasma norepinephrine concentration in either group. Thus, in patients with essential hypertension, cilnidipine suppressed cardiac sympathetic overactivity and amlodipine had a little suppressive effect. Cilnidipine may provide a new strategy for treatment of cardiovascular diseases with sympathetic overactivity.

Adult↗
PubMedDate not supplied

Interest of the association clonidine-spironolactone in cirrhotic patients with ascites and activation of sympathetic nervous system.

BACKGROUND: The aim of this study was to examine the effects of spironolactone, clonidine and the association of clonidine-spironolactone on renin-aldosterone and sympathetic systems, renal function, systemic hemodynamics and mobilization of ascites in 32 alcoholic cirrhotic patients with marked increase in sympathetic system. METHODS: Measurements were taken before and after an 8-day treatment with spironolactone (200 mg/day), after an 8-day treatment with clonidine (0.150 mg/day) and 10 days after adjunction of spironolactone (200 mg/day) to clonidine. RESULTS: Three patients abandoned the treatment or were excluded because lack of compliance. Spironolactone alone induced an increase in renin-aldosterone and sympathetic systems without any remarkable increase of natriuresis and body weight loss. Given for 8 days, clonidine alone induced a significant decrease in plasma norepinephrine associated with a significant increase in glomerular filtration rate without effect on natriuresis. In contrast, 10 days after adjunction of spironolactone to clonidine, plasma renin and aldosterone significantly decreased, natriuresis increased (from 7.4 +/- 0.7 to 41.6 +/- 3.2 mEq/24 h) and body weight decreased (from 66.03 +/- 2.3 to 63.5 +/- 2.3 kg) without adverse effects. CONCLUSION: In cirrhotic patients with ascites and marked activation of sympathetic nervous system, spironolactone (200 mg/day) is unable to mobilize ascites. In these patients, after 8 days, clonidine decreases sympathetic activity, increases glomerular filtration rate and after 18 days, decreases plasma renin and aldosterone concentrations allowing a better action of spironolactone. The association clonidine-spironolactone enhances natriuresis and body weight loss.

Adrenergic alpha-Agonists↗
PubMed1998

Peripheral vascular tone in patients with cirrhosis: role of the renin-angiotensin and sympathetic nervous systems.

OBJECTIVE: The aims of the study were to establish the roles of angiotensin II and of the cardiopulmonary baroreceptor reflex in the regulation of peripheral vascular tone in patients with cirrhosis. METHODS: Forearm blood flow responses to subsystemic, locally active intrabrachial infusions were measured in patients with Child's Grade C cirrhosis and matched controls using bilateral venous occlusion plethysmography. Responses were determined to the angiotensin II type I receptor antagonist, losartan, noradrenaline, angiotensin II and the nitric oxide synthase inhibitor, L-NG-monomethyl arginine. RESULTS: Losartan at 30 and 90 micrograms/min caused no significant change in blood flow in controls, but caused 23 +/- 6% and 27 +/- 5% increases in patients respectively (p < 0.001). Lower body negative pressure caused a mean bilateral reduction in forearm blood flow of 20 +/- 4% in controls (p < 0.001) but only tended to reduce flow (9 +/- 5%; p = 0.06) in patients (p < 0.001; controls vs. patients). Noradrenaline, angiotensin II and L-NG-monomethyl arginine caused significant vasoconstriction (p < 0.001) in both patients and controls although angiotensin II caused significantly less vasoconstriction in patients (p = 0.01). CONCLUSIONS: We conclude that angiotensin II makes an important contribution to basal peripheral vascular tone in patients with cirrhosis in the face of reduced vascular responses to its local administration. In addition, the vasoconstrictor response to cardiopulmonary baroreceptor unloading is attenuated despite normal vascular responses to noradrenaline. These responses are consistent with chronic activation of the renin-angiotensin and sympathetic nervous systems in patients with advanced cirrhosis.

Analysis of Variance↗
PubMed1994

Involvement of the sympathetic nervous system in antihypertensive effect of cicletanine in salt-loaded young spontaneously hypertensive rats.

We examined the role of the sympathetic nervous system in the antihypertensive effect of long-term (4-week) administration of cicletanine (50 mg/100 g in diet) in young (6 week-old) spontaneously hypertensive rats (SHR) fed an 8.0% salt-containing diet. Salt loading accelerated the development of hypertension in young SHR (mean blood pressure [BP]: 158 +/- 3 v 196 +/- 5 mm Hg, P < .01). Although cicletanine did not affect mean BP in non-salt-loaded SHR, it reversed salt-induced hypertension (155 +/- 3 mm Hg, P < .01). Salt loading elevated plasma norepinephrine (NE) (246 +/- 16 v 451 +/- 87 pg/mL, P < .05) but simultaneous administration of cicletanine inhibited the increase in plasma NE with salt loading (234 +/- 12 pg/mL, P < .01). Hexamethonium, a ganglionic blocking agent, produced a greater hypotensive effect in salt-loaded than in non-salt-loaded SHR (-40 +/- 4 v -78 +/- 4 mm Hg, P < .01). In salt-loaded SHR with cicletanine, however, the hypotensive effect of hexamethonium was suppressed compared with salt-loaded SHR without cicletanine (-52 +/- 4 mm Hg, P < .01). Both plasma NE (r = 0.608, P < .01) and decrease in mean BP with hexamethonium (r = -0.798, P < .01) correlated with baseline mean BP. Thus, cicletanine inhibited the salt-induced rise in mean BP of young SHR, possibly through the suppression of enhanced sympathetic nerve activity.

Animals↗
PubMed1990

Development of the sympathetic nervous system response to endotoxicosis in the rat: importance of non-baroreflex mechanisms in pre-weanlings and adults.

The sympathetic nervous system response to endotoxicosis was studied in the rat at ages before (11-12 days) and after (19-20 days) maturation of the baroreflex and in adults by recording preganglionic impulses during i.v. infusions of endotoxin (S. enteriditis). At all ages, the discharge rate increased before there was any decrease in arterial blood pressure. The magnitude of the increase (65%) was the same in 11-12 days-old and adult rats while 19-20 days-old rats were hyperactive (278% increase). Subsequently, in the hypotensive phase of the endotoxicosis (diastolic pressure decrease 50-60%) there was an additional increase in discharge in the 19-20 days- old rats (43% and in adults (70%) but not in 11-12 days-old rats. The hypotensive discharge rate of the 11-12 days-old rat reached only 20% of the maximum; it reached 80% in the hyperactive 19-20 days-old rat and 65% in adults. At all ages, the elevated hypotensive discharge rate persisted after steady state blood pressure was raised by infusing dextran. The discharge rate was diminished transiently during pressor responses to accelerated infusion or bolus injections of dextran. The conclusions are: (i) endotoxic stimulation of sympathetic outflow is initiated by a non-baroreflex mechanism in adult as well as in pre-weaning rats; (ii) there is added stimulation during hypotension after the baroreflex is mature, but (iii) the non-baroreflex stimulation continues to excite the preganglionic neurons and obtunds baroreflex feedback inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2003

Activation of the peripheral sympathetic nervous system increased the expression of cyclooxygenase-2 (COX-2) mRNA in mouse calvaria.

Pharmacological stimulation of adrenoceptor was demonstrated to increase the synthesis of prostaglandin (PG)-E(2), well known to modulate bone metabolism by regulating development and function of osteoclasts and osteoblasts, in cultured osteoblastic cells. Recently, intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS), which caused the inflammatory stimuli in the brain, was demonstrated to increase the outflow of the peripheral sympathetic nervous system. In this study, to clarify the physiological role of sympathetic nerves to bone metabolism in vivo, we examined the effect of LPS (i.c.v.) on the expression of cyclooxygenase-2 (COX-2) mRNA in mouse calvaria, using reverse transcription-polymerase chain reaction analysis. The expression of COX-2 mRNA was increased by LPS (i.c.v.) in mouse calvaria. The treatment with the neurotoxin 6-hydroxydopamine or beta-blocker inhibited the central LPS-induced COX-2 mRNA in mouse calvaria. In addition, the treatment of calvaria with isoprenaline, beta-agonist, or noradrenaline increased PGE(2) synthesis in the organ culture system. These findings show that central LPS-induced COX-2 mRNA was mediated by the activation of postganglionic sympathetic nerve fibers and beta-adrenoceptor in mouse calvaria and suggest that in vivo activation of the sympathetic nervous system modulates bone metabolism.

Animals↗