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Results for “Sympathetic Nervous System”

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At least 73 records · Page 4Linked to original sources
PubMed2001

The peripheral sympathetic nervous system in human obesity.

The peripheral sympathetic nervous system is a key factor in the regulation of energy balance in humans. Differences in sympathetic nervous system activity may contribute to variations in 24 h energy expenditure between individuals. beta-Adrenoceptors play a more important role than alpha-adrenoceptors in this regulation. The involvement of both beta 1- and beta 2-adrenoceptor subtypes has been demonstrated, the role of the beta 3-adrenoceptor subtype is not yet clear. Normal or increased levels of sympathetic nervous system activity and reduced reactivity appear to be present in established obesity. Furthermore, the sensitivity for beta-adrenoceptor stimulation is impaired in obesity. The blunted reactivity and sensitivity may contribute to the maintenance of the obese state. There are data to suggest that they may also play a role in the aetiology of obesity, because the impairments often remain after weight reduction. Furthermore, a negative correlation between baseline sympathetic nervous system activity and weight gain during follow-up has been found in Pima Indians. Recently, genetic evidence about the involvement of adrenoceptors in obesity has become available. Although the results of association and linkage studies on polymorphisms in the beta 2-, beta 3- and alpha 2-adrenoceptor genes are inconsistent, the functional correlates of some of these polymorphisms (changes in agonist-promoted down-regulation, protein expression levels, lipolytic sensitivity, basal metabolic rate, sympathetic nervous system activity) suggest that they may be important in the aetiology of obesity.

Energy Metabolism↗
PubMed1997

Quantitative evaluation of sympathetic nervous system dysfunction in patients with reflex sympathetic dystrophy.

The sympathetic nervous system function in 20 patients with reflex sympathetic dystrophy (RSD) of one upper extremity was examined by a non-invasive laser Doppler method to assess fingertip blood flow and vasoconstrictor response to deep inspiration. We observed an increased blood flow but an unchanged vasoconstrictor response in the affected hand in stage 1 of the disorder, but in stage 2 there was a decreased blood flow and a stronger vasoconstriction following an inspiratory gasp. Skin blood flow and vasoconstrictor response returned to normal following successful treatment of the condition. These results suggest that in RSD patients the sympathetic nervous system function is altered and is different in the various stages. The objective method used in our study may be of value in the diagnosis and management of RSD.

Adult↗
PubMedDate not supplied

Calcium channel blockade with nitrendipine. Effects on sodium homeostasis, the renin-angiotensin system, and the sympathetic nervous system in humans.

To test the hypothesis that the antihypertensive effect of the calcium channel blocking drug nitrendipine is in part related to natriuresis, we gave 16 subjects (8 normal, 8 hypertensive) placebo for 8 days followed by nitrendipine titrated to 20 mg twice daily for 8 days. The same diet was prepared for each meal for the entire study. Sodium intake was fixed for each subject and averaged 150 mEq/day. All urine was collected every day. Blood was drawn at the end of the placebo and nitrendipine periods for renin, aldosterone, and norepinephrine values. Nitrendipine caused a significant increase (p less than 0.05) in cumulative sodium excretion of 161 mEq over 7 days in the normal subjects and 103 mEq in hypertensive subjects. Potassium excretion was unaffected. In both hypertensive and normal subjects, plasma renin and plasma norepinephrine activity increased significantly (p less than 0.05), while plasma aldosterone levels did not change. Upright systolic blood pressure decreased significantly (p less than 0.05) in both groups, whereas upright diastolic blood pressure decreased only in hypertensive subjects. We conclude that blood pressure lowering effects of this drug may be in part related to natriuresis and that calcium channel blockade may dissociate plasma renin activity from that of aldosterone.

Adult↗
PubMed1997

Target-independent cholinergic differentiation in the rat sympathetic nervous system.

Chemical coding in the sympathetic nervous system involves both noradrenergic and, for a minority of neurons, cholinergic neurotransmission. The expression of the cholinergic phenotype in the developing sympathetic nervous system was examined to determine if coding for cholinergic transmission occurs before or after innervation of peripheral target organs. The vesicular acetylcholine transporter (VAChT) and choline acetyltransferase, the products of the "cholinergic gene locus" determining the cholinergic phenotype, were expressed in principal cells of the paravertebral, but only rarely in prevertebral, sympathetic chains as early as embryonic day 14. A subpopulation of VAChT- and choline acetyltransferase-positive sympathetic ganglion cells persisted throughout development of the stellate and more caudal paravertebral ganglia into anatomically distinct cell groups, and into adulthood. The forepaw eccrine sweat glands, innervated exclusively by the stellate ganglion, received VAChT-positive nerve terminals at least as early as postembryonic day 4, coincident with the development of the sweat glands themselves. These terminals, like the VAChT-positive cell bodies of the developing stellate ganglion, have some noradrenergic traits including expression of tyrosine hydroxylase, but did not express the vesicular monoamine transporter, and are therefore not functionally noradrenergic. Development of the cholinergic phenotype in principal cells of the sympathetic paravertebral ganglia apparently occurs via receipt of instructive cues, or selection, within the sympathetic chain itself or perhaps even during migration of the cells of the neural crest from which the paravertebral ganglia arise.

Animals↗
PubMed1989

Sympathetic nervous system activity and the heart.

The sympathetic nervous system has been viewed as the critical mechanism for cardiovascular response to increased circulatory needs during acute stress, augmenting cardiac rate and contractility and changing peripheral vascular tone. These physiologic responses, however, are increasingly thought to cause long-term adverse effects--such as altered myocardial function; renal, systemic, and coronary vasoconstriction; ventricular arrhythmias; and left ventricular hypertrophy--for some patients with cardiovascular disease. How the sympathetic nervous system affects the pathophysiology of cardiovascular diseases is not fully understood, although new techniques for assessing plasma catecholamines and for quantitating sympathetic activity are adding to our knowledge. Nevertheless, a review of the physiologic responses to sympathetic nervous system stimulation reveals much about their possible role in the cardiovascular disease process.

Animals↗
PubMed1992

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure.

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

Adrenal Medulla↗
PubMed1975

Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon. Influence of the sympathetic nervous system.

The influence of the sympathetic nervous system on the cerebral circulatory response to graded reductions in mean arterial blood pressure was studied in anesthetized baboons. Cerebral blood flow was measured by the 133Xe clearance method, and arterial blood pressure was decreased by controlled hemorrhage. In normal baboons, the constancy of cerebral blood flow was maintained until mean arterial blood pressure was approximately 65% of the base-line value; thereafter, cerebral blood flow decreased when arterial blood pressure was reduced. Superior cervical sympathectomy of 2-3 weeks duration did not affect the normal response. In contrast, both acute surgical sympathectomy (cervical trunk division) and alpha-receptor blockade (1.5 mg/kg of phenoxybenzamine) enhanced the maintenance of cerebral blood flow in the face of hemorrhagic hypotension in that cerebral blood flow did not decrease until mean arterial blood pressure was approximately 35% of the base-line value. The results indicate that the sympathetic nervous system is not involved in the maintenance of cerebral blood flow in the face of a fall in arterial blood pressure. Indeed, the implication is that the sympathicoadrenal discharge accompanying hemorrhagic hypotension is detrimental to, rather than responsible for, cerebral autoregulation.

Adrenergic alpha-Antagonists↗
PubMed1987

The enhancement of the immune response by pain stimulation in mice. I. The enhancement effect on PFC production via sympathetic nervous system in vivo and in vitro.

Effects of catecholamines and osmotical and physical stimuli on the induction of anti-sheep red blood cells (SRBC) plaque-forming cells (PFC) were investigated in (C57BL/6 X BALB/c)F1 mice in vivo and in vitro. The anti-SRBC PFC from mice immunized with 5 X 10(7) SRBC was markedly increased by daily s.c. injections of epinephrine. The enhancement of PFC by epinephrine was completely blocked by preadministration with propranolol and hexamethonium, but not with phentolamine. The PFC was increased by osmotic and physical stimuli given once a day for 4 days after immunization with SRBC. The enhancement of PFC by these stimuli was completely blocked by preadministration with propranolol and hexamethonium. The enhancement of PFC by physical stimuli was observed in nonimmunized mice when spleen cells from stimulated mice were cultured with SRBC in vitro. In normal mice, the enhancement of PFC was observed 2 hr after one physical stimulation. However, spleen cells from mice given two physical stimuli did not show the enhancement of PFC after treatment with anti-Thy-1.2 antibody and complement, nor after removal of nonadherent cells. Next, the serum obtained from mice 30 to 60 min after a physical stimulation enhanced PFC of normal mice spleen cells in vitro, but the enhancement was abolished by the addition of propranolol. The enhancement of anti-SRBC PFC by s.c. injection of epinephrine suggested that the autonomic nervous system, especially the sympathetic nervous system, was activated by a local stimulus effect of the injection. This enhancement of anti-SRBC PFC appear to be due to the activation of antigen non-specific helper T lymphocytes by the beta-actin of endogenous catecholamines from the adrenal gland.

Animals↗
PubMed1984

[The effects of the intracerebroventricular administration of 5-hydroxytryptamine on hemodynamics in conscious rats. Participation of the serotonin receptor and the sympathetic nervous system].

We have previously reported that the intracerebroventricular (i.c.v.) administration of 5-hydroxytryptamine (5-HT) in conscious rats elicited significant pressor response, which was accompanied with an increase in plasma norepinephrine and the pressor response, was abolished by peripheral phenoxybenzamine pretreatment. For further investigation of the relationship between the serotonergic nervous system and the sympathetic nervous system, the effect of either i.c.v. or intravenous (i.v.) serotonin receptor antagonist, methysergide pretreatment on hemodynamic response to centrally administrated 5-HT was studied. Male Wistar rats weighing approximately 250g were used. On the day before the study, the unilateral carotid artery was cannulated (PE-50) to facilitate mean arterial pressure (MAP) and pressure triggered heart rate (HR) observation. Also, a cannula (PE-10) was inserted stereotaxically into the anterior horn of the lateral cerebral ventricle. The experiment was performed under a conscious and minimumly restrained state. After the observation of resting MAP and HR for at least 20 minutes, 5 microgram of 5-HT was given i.c.v. and MAP and HR were recorded for 50 minutes. Then, the rats were divided into two groups, one group (n = 9) received 1 microgram of i.c.v. methysergide and the other group (n = 10) received 1 mg/kg of i.v. methysergide. Ten minutes after either methysergide i.c.v. or i.v. treatment, 5 microgram of 5-HT was administrated i.c.v. again, and MAP and HR were observed for 30 minutes. Resting MAP and HR were 101.6 +/- 3.0mmHg and 413.8 +/- 20.0/min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Migraine: a chronic sympathetic nervous system disorder.

OBJECTIVES: To determine the degree of diagnostic and clinical similarity between chronic sympathetic nervous system disorders and migraine. BACKGROUND: Migraine is an episodic syndrome consisting of a variety of clinical features that result from dysfunction of the sympathetic nervous system. During headache-free periods, migraineurs have a reduction in sympathetic function compared to nonmigraineurs. Sympathetic nervous system dysfunction is also the major feature of rare neurological disorders such as pure autonomic failure and multiple system atrophy. There are no known reports in the medical literature, however, comparing sympathetic nervous system function in individuals with migraine, pure autonomic failure, and multiple system atrophy. METHODS: A detailed review of the literature was performed to compare the results of a wide variety of diagnostic tests and clinical signs that have been described in these 3 heretofore unrelated disorders. RESULTS: The data indicate that migraine shares significant diagnostic and clinical features with both pure autonomic failure and multiple system atrophy, yet represents a distinct subtype of chronic sympathetic dysfunction. Migraine is most similar to pure autonomic failure in terms of reduced supine plasma norepinephrine levels, peripheral adrenergic receptor supersensitivity, and clinical symptomatology directly related to sympathetic nervous system dysfunction. The peripheral sympathetic nervous system dysfunction is much more severe in pure autonomic failure than in migraine. Migraine differs from both pure autonomic failure and multiple system atrophy in that migraineurs retain the ability, although suboptimal, to increase plasma norepinephrine levels following physiological stressors. CONCLUSIONS: The major finding of the present study is that migraine is a disorder of chronic sympathetic dysfunction, sharing many diagnostic and clinical characteristics with pure autonomic failure and multiple system atrophy. However, the sympathetic nervous system dysfunction in migraine differs from pure autonomic failure and multiple system atrophy in that occurs in an anatomically intact system. It is proposed that the sympathetic dysfunction in migraine relates to an imbalance of sympathetic co-transmitters. Specifically, it is suggested that a migraine attack is characterized by a relative depletion of sympathetic norepinephrine stores in conjunction with an increase in the release of other sympathetic cotransmitters such as dopamine, prostaglandins, adenosine triphosphate, and adenosine. An enhanced understanding of the sympathetic dysfunction in migraine may help to more effectively diagnose, prevent, and/or treat migraine and other types of headache.

Autonomic Nervous System Diseases↗
PubMed2000

Role of the sympathetic nervous system in human renovascular hypertension.

The findings in humans as to whether elevated sympathetic nerve activity contributes to renovascular hypertension have been less consistent compared with the results obtained in experimental models of renovascular hypertension. Collectively, there are several lines of evidence to support the view that sympathetic nerve activity is elevated in patients with renovascular hypertension. It is uncertain, however, whether this adrenergic overactivity is specific for renovascular hypertension per se, or the cause of severe hypertension with target organ damage. Central or peripheral stimulation of sympathetic nerve activity by angiotensin II, or stimulation of central sympathetic outflow via afferent renal nerves of ischemic kidneys, are possible mechanisms to explain the elevated sympathetic nerve activity in renovascular hypertension. Therapy that diminishes the activity of the sympathetic nervous system and the renin-angiotensin system seems rational and could perhaps also improve the poor prognosis for these patients.

Adrenergic Fibers↗
PubMed1998

Identification of cardiovascular pathways in the sympathetic nervous system.

1. Sympathetic autonomic neurons show distinct patterns of expression of a range of neurochemicals that can be detected immunohistochemically. Often, functionally homologous neurons in the autonomic nervous system express identical combinations of substances that serve as a chemical code that allows them to be identified among other autonomic neurons. 2. In the rat stellate ganglion, where many neurons express either immunoreactivity (IR) to neuropeptide Y (NPY) or the calcium-binding protein calbindin, a population of large post-ganglionic neurons found along the medical border of the stellate ganglion, around the origin of the cardiac nerves, expressed intense IR to both substances at all ages examined, from early postnatal to adult. 3. In the heart, in the first few postnatal weeks, many nerve terminals were IR for both NPY and calbindin, but, with increasing age, calbindin-IR was progressively lost from NPY-IR terminals. Nerve terminals IR for both calbindin and NPY were not seen around pulmonary blood vessels or in the trachea or the thymus. 4. Nerve terminals IR for calretinin, another calcium-binding protein, were present in dense pericellular baskets around neurons in the stellate IR for both calbindin and NPY. The terminals also contained nitric oxide synthase (NOS)-IR. 5. It is suggested that the calbindin- and NPY-IR neurons in the stellate ganglion are the post-ganglionic neurons that innervate the heart and that the nerve terminal containing calretinin and NOS-IR that surround them are the cardiac preganglionic terminals. It thus appears possible, in the rat, to identify the sympathetic cardiac pathway arising in the spinal cord and controlling the heart purely on the basis of chemical coding.

Animals↗
PubMed1985

Total and renal sympathetic nervous system activity in alcoholic cirrhosis.

Basal sympathetic nervous system activity was assessed in 8 unmedicated patients with alcoholic cirrhosis using a previously developed radiotracer method for measuring total and renal noradrenaline release to, and clearance from, plasma. Compared to the control group total noradrenaline clearance was significantly increased in the patients with advanced alcoholic cirrhosis (Pugh grade C) [1.89 +/- 0.13 vs 1.51 +/- 0.11 l/min, P less than 0.05) indicating that endogenous plasma noradrenaline levels underestimate total sympathetic nervous system activity in these patients. Renal noradrenaline clearance was similar to controls independent of the severity of the liver disease. Both total and renal noradrenaline release were significantly increased in the patients with cirrhosis. The ratio of renal to total noradrenaline release was similar in cirrhotic (26 +/- 7%) and control (23 +/- 5%) groups. Increased arterial plasma adrenaline levels, indicative of adrenal medullary stimulation, were also evident in the patients with cirrhosis and correlated significantly with total noradrenaline spillover (r = 0.732, P less than 0.05). These results strongly suggest that in patients with cirrhosis, rather than a preferential increase in renal sympathetic tone, the increase is part of a pattern of generalized sympathoadrenomedullary activation. Although renal renin secretion was significantly increased in the cirrhotic group no correlation with renal noradrenaline release was seen (r = 0.199), raising the possibility that in cirrhosis renal sympathetic tone is not a major determinant of renal renin secretion. Finally, renal noradrenaline release did not correlate with renal blood or plasma flow but an influence of the sympathetic nervous system on renal function was suggested by the correlation observed between total noradrenaline spillover and impaired salt (r = -0.683, P less than 0.05) and water excretion (r = -0.702, P less than 0.05) demonstrated in the cirrhotic patients.

Adrenal Medulla↗
PubMed1995

Role of the sympathetic nervous system in acute pain and inflammation.

The sympathetic nervous system serves not only to regulate involuntary functions, but also appears to play an important part in modulating sensory processing. While studies in animal models of neuropathic pain and clinical observations point to a role of the sympathetic nervous system in certain chronic pain states, the function of the sympathetics in postoperative pain and inflammation is debatable. Behavioural studies in rats point to a contribution of the sympathetic postganglionic terminal in the hyperalgesia of cutaneous inflammation and the severity of arthritis. An indirect effect of noradrenaline and inflammatory mediators via the release of prostaglandins has been postulated. Neurophysiological studies of nociceptors in rats and psychophysical studies in humans have failed to provide confirmatory evidence for the role of the sympathetic efferents in inflammatory pain and hyperalgesia. The clinical significance of the potential interaction of the sympathetic nervous system and the somatic afferent system needs further investigation.

Acute Disease↗