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Results for “Sympathetic Nervous System”

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PubMed2003

The role of the sympathetic nervous system in anxiety: Is it possible to relieve anxiety with endoscopic sympathetic block?

The function of the autonomic nervous system is divided so that the parasympathetic system spares central nervous system energy and the sympathetic system makes extra energy available and consumes it. The sympathetic nervous system then prepares our body for emergency and it always functions when our conscious or even unconscious mind notices a need for defence or to provide energy. A surgical procedure, where the upper thoracic sympathetic ganglions are ablated, either with cauterization or clamping with metallic clips, has been used to treat sweating of the hands and facial blushing for decades. Instead of ablating large areas of sympathetic trunk, which can cause severe side-effects such as reflex sweating of the body, the surgical procedure is nowadays carried out in a more precise symptom-mediating level of uppermost thoracic sympathetic ganglia. Blushing, hyperhidrosis of palms and head, and trembling are common in social phobia, and they seem to be provoked by the activation of the sympathetic nervous system. Preliminary studies show that some social phobia patients may benefit from the endoscopic sympathetic block (ESB). If the patient with generalized social phobia has not received help with adequate medication or psychotherapy, the ESB may be a new possible treatment of choice.

Anxiety Disorders↗
PubMed1987

Inhibitory control of proximal colonic motility by the sympathetic nervous system.

The purpose of this study is to determine whether or not the sympathetic nervous system provides a tonic inhibitory input to the colon in chloralose-anesthetized cats. Proximal and midcolonic motility were monitored using extraluminal force transducers. An intravenous bolus injection of 5 mg of phentolamine in 14 animals elicited a pronounced increase in proximal colon contractility. The minute motility index changed from 0 +/- 0 to 26 +/- 4 after phentolamine administration. Midcolonic motility also increased in response to phentolamine. Specific blockade of alpha 2-receptors, but not alpha 1-receptors, caused the same response seen with phentolamine. alpha-Adrenergic blockade increased colon contractility after spinal cord transection but not after ganglionic blockade. Blockade of alpha-adrenergic receptors was also performed before vagal and pelvic nerve stimulation and in both cases increased colonic motility. Vagal stimulation alone had no effect on colonic contractility, while pelvic nerve stimulation increased motility at the midcolon. alpha-Receptor blockade did not alter the ineffectiveness of vagal stimulation but did unmask excitatory effects of pelvic nerve stimulation on the proximal colon. All excitatory colonic responses were prevented by blocking muscarinic cholinergic receptors. These data indicate that tonic sympathetic nervous system activity exerts an inhibitory effect on colonic motility. The inhibitory effect is mediated through alpha 2-adrenergic receptors. Based on these findings, we suggest that alterations in sympathetic nervous system activity may be extremely important for the regulation of circular muscle contractions in the colon.

Acetylcholine↗
PubMed1979

Dysfunction of the sympathetic nervous system in tetanus. A study of 3 cases.

In severe cases of tetanus an overactivity of the sympathetic nervous system has been postulated because of the clinical symptoms including hypertension, fluctuating blood pressure, tachycardia, tachyarrhythmia and peripheral vasoconstriction. In the present study the involvement of the sympathetic nervous system in tetanus was investigated by serial determinations of plasma adrenaline (A) and noradrenaline (NA) in 2 patients who developed severe symptoms of tetanus and the characteristic cardiovascular disturbances. Sustained high circulating levels of NA and A could be observed indicating a prolonged overactivity of the sympathetic nervous system. In one case, the elevation of the NA level in plasma persisted until the disturbances of the motor nervous system ceased. In a third case of tetanus without cardiovascular abnormalities, the plasma NA and A only increased slightly on a few occasions. The results demonstrate that an overactivity of the sympathetic nervous system can complicate the course of severe tetanus.

Adult↗
PubMed2001

[The glial cell in the ontogenesis of the human peripheral sympathetic nervous system and in neuroblastoma].

The developmental role of glial cells in the human peripheral sympathetic nervous system is still unclear. Immunohistochemical studies on human embryos and fetuses reveal that the migrating clusters of undifferentiated neuroblasts contain sustentacular cells and are completely separated from adjacent tissues by a peripheral layer of Schwann-like cells and continuous basement membrane. This topographic distribution seems to be strategic and suggests a role of glial cells and extracellular matrix in migration and differentiation processes of undifferentiated neuroblasts. A similar distribution pattern between glial cells/extracellular matrix and neuroblasts can be observed in neuroblastomas exhibiting a microscopic nodular growth pattern, providing additional evidence that neuroblastoma represents an arrest in the differentiation/maturation of cells during the ontogenesis of the human peripheral sympathetic nervous system. Although it is commonly believed that Schwann cells in neuroblastoma arise from cells "infiltrating neoplasia", arising from peripheral nerves adjacent tumor, our ontogenetic findings suggest that the glial cell component of neuroblastoma derives from that normally associated with developing neuroblasts. We discuss the normal development of the three lineages of the human peripheral sympathetic nervous system (ganglial, neuroendocrine or chromaffin, and glial), with special emphasis on glial cells and extracellular matrix components and on the comparison between ontogenesis and neuroblastoma.

Basement Membrane↗
PubMed1984

Effect of antihypertensive therapy on sympathetic nervous system activity in patients with essential hypertension.

The sympathetic nervous system (SNS) plays a major role in blood pressure regulation. Although the exact relationship of the SNS to the etiology of hypertension remains undetermined, many of the agents used to treat hypertension interfere with this system. Clonidine, methyldopa, guanethidine, and reserpine decrease SNS tone whereas hydralazine, minoxidil, and hydrochlorothiazide increase it. Most evidence suggests that beta-adrenergic blocking agents decrease SNS activity. The effect of prazosin and captopril on the SNS requires further study. The appropriate use of these antihypertensive agents requires a knowledge of their sites of action and the physiological reflexes they induce. Efficacy, toxicity, and effective drug combinations can be predicted based on their mechanism of action and effect on SNS activity.

Antihypertensive Agents↗
PubMed1985

Influence of the sympathetic nervous system on the growth of neuroblastoma in vivo and in vitro.

The sympathetic nervous system exerts a trophic-mitogenic influence on C-1300 mouse neuroblastoma. We now report that sympathetic axotomy suppresses growth of the S-20 clonal line of neuroblastoma but does not influence the growth in vivo of two other clonal lines, NIE-115 and C-46. Sympathetic ganglia-conditioned medium significantly increases proliferation of S-20 cells in vitro. Growth of NIE-115 and C-46 clonal neuroblastoma lines is not influenced by sympathetic ganglia-conditioned medium. We postulate that the sympathetic nervous system secretes a mitogenic-trophic factor that favors growth of C-1300 neuroblastoma in vivo. Sensitivity to this factor varies between neuroblastoma clonal lines.

Animals↗
PubMed2004

Morphology of experimentally induced tumors of the sympathetic nervous system in rats.

Seventeen tumors of the sympathetic nervous system were discovered in offspring of rats exposed in utero at a single dose of 80mg/kg of N-nitrosoethylurea at the day 16-19 of pregnancy, and then to constant light regimen. These tumors were classified as follows: benign--ganglioneuroma (six cases) and malignant--ganglioneuroblastoma (four cases) and neuroblastoma (seven cases). The most frequent location was in the sympathetic trunk in the mediastinum and in the retroperitoneal space. Morphological features of these induced tumors represent a model for similar neoplasms in humans in childrens' age.

Animals↗
PubMed1994

Differential effects of dietary fats on sympathetic nervous system activity in the rat.

Fat feeding stimulates sympathetic nervous system (SNS) activity in rats. To determine if fats vary in their potency as stimulants of the SNS, [3H]norepinephrine ([3H]NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of animals fed lab chow diets supplemented with safflower oil, coconut oil, or medium-chain triglycerides (MCT). At 5 days, all three fats accelerated [3H]NE turnover in heart and did so equally, but only when the fat supplement represented an increase in energy intake. However, after 14 days, safflower oil and coconut oil but not MCT increased [3H]NE turnover in heart compared with turnover rates obtained in animals fed isoenergetic amounts of chow. Furthermore, the stimulatory effect of safflower oil on [3H]NE turnover was statistically greater than that seen in animals fed equivalent amounts of coconut oil. In vivo synthesis of NE assessed by accumulation of dopamine (DA) in heart following inhibition of dopamine-beta-hydroxylase (D beta H) was likewise highest in safflower oil-fed rats and lowest in those fed MCT. Thus, sympathetic activation by dietary fat varies among different fats, suggesting a role for fatty acid intake in dietary regulation of the SNS.

Adipose Tissue↗
PubMed1994

Effects of chronic lard feeding on sympathetic nervous system activity in the rat.

The level of sympathetic nervous system (SNS) activity in obesity is controversial, with reports claiming either increased or decreased SNS activity. The following studies examined SNS activity in a dietary form of obesity, ingestion of a lard-enriched diet for 4 wk. Plasma norepinephrine (NE) levels were 61% higher in rats fed the lard-enriched diet than in chow-fed controls at 20 degrees C (200 +/- 24 pg/ml vs. 124 +/- 6, P < 0.005) and remained elevated after 1 h of cold exposure (4 degrees C). [3H]NE turnover was markedly increased in heart, but not in interscapular brown adipose tissue (IBAT), kidney, liver, skeletal muscle, or spleen of rats fed the high-fat diet. By contrast, ingestion of a diet similarly enriched with sucrose raised rates of [3H]NE turnover in IBAT as well as in heart. Thus chronic ingestion of a lard-enriched diet induces region-specific stimulation of SNS activity that is greater in heart than in IBAT. Whereas the absence of an SNS response to lard in IBAT may contribute to weight gain in these animals, activation of cardiac sympathetic nerves may promote development of hypertension in this model of obesity.

Acclimatization↗
PubMed2007

Modulation operated by the sympathetic nervous system on jaw reflexes and masticatory movement.

The sympathetic nervous system (SNS), that is activated under condition of physical, psychological and psychosocial stress, affects force production and fatigability of muscles by controlling both muscle blood flow and the intracellular contractile mechanism. In addition SNS may affect motor function by modulating afferent activity from muscle spindles that are highly concentrated in jaw-closing muscles. Possible implications of these actions on masticatory function and myofascial pain are discussed.

Electromyography↗
PubMedDate not supplied

Contribution of vasopressin and the sympathetic nervous system in the early phase of high sodium one-kidney renal hypertension.

This study assessed the contributions of the sympathetic nervous system and arginine vasopressin to the onset of one-kidney, one-wrap (1K1W) renal hypertension in rats fed a high sodium diet. Two weeks before renal wrap or sham wrap, rats were given a high sodium diet and water ad libitum. At 3 days postwrap, resting mean arterial pressure (MAP) was significantly greater in renal-wrapped rats. The contributions of the sympathetic nervous system and vasopressin to blood pressure (BP) were assessed by ganglionic blockade and vascular vasopressin receptor antagonism, respectively. Depressor responses to ganglionic blockade were significantly greater in the normotensive rats as compared to the hypertensive rats. Administration of vasopressin antagonist caused a significant fall in pressure only in wrapped rats. In addition, enhanced pressor responses to bolus injections of vasopressin were observed in hypertensive rats. These results indicate that during this phase of the hypertension there is an activation of the vasopressin pressor system without an increase in neurogenic function. Equalization of arterial pressure occurred only when both systems were blocked, regardless of the order of blockade, which indicated that the sympathetic nervous system and vasopressin interact to maintain the hypertension. Comparison of depressor responses to the blocking agents revealed that the interaction is compensatory in nature since the contributions of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure were greater when the other system was blocked.

Angiotensin II↗
PubMed1991

Relation of obesity and diet to sympathetic nervous system activity.

The hypothesis that dietary intake and obesity stimulate the sympathetic nervous system was investigated in a cross-sectional study of 572 men aged 43-85 years from the Normative Aging Study. Habitus was represented by body mass index, as a measure of overall adiposity, and by the ratio of abdomen-to-hip circumference (abdomen/hip ratio), as a measure of centripetal fat distribution. Sympathetic activity was assessed by measurement of 24-hour urinary norepinephrine excretion. Increased body mass index and total caloric intake were independently associated with increased 24-hour urinary norepinephrine excretion (p = 0.0001 and p = 0.0055, respectively). In addition, mean urinary norepinephrine excretion was higher in subjects classified as either hyperglycemic (serum fasting glucose greater than or equal to 113 mg/dl) and hyperinsulinemic (serum fasting insulin greater than or equal to 19 microIU/ml) (p = 0.0023) or in subjects classified as either hyperglycemic or hyperinsulinemic (p = 0.0063) than the mean urinary norepinephrine excretion in normal subjects. These relations were demonstrated to be independent of age, smoking status, and physical activity. Our results are consistent with the hypothesis that insulin mediates sympathetic stimulation in response to dietary intake and increases sympathetic nervous system activity in the obese.

Adipose Tissue↗
PubMed1989

Oxygen consumption after massive sympathetic nervous system discharge.

We evaluated the possibility that massive, sympathetic nervous system (SNS) activation [as may precede the development of neurogenic pulmonary edema (NPE)] increases O2 demand. O2 consumption (VO2) and plasma concentrations of the calorigenic agents, epinephrine (EPI) and norepinephrine (NE) were measured in alpha-chloralose-anesthetized dogs under control conditions and for 3 h after the administration of either 1) intracisternal (ic) veratrine to activate the SNS, 2) intravenous (iv) veratrine, 3) ic saline, or 4) ic veratrine, after clamping the adrenal blood vessels. VO2 increased 31.7 +/- 3.6% (SE), and EPI and NE increased to, respectively, 30,853 +/- 8,347 and 8,176 +/- 2,104 pg/ml in the ic veratrine group. No increases in VO2 and EPI and attenuated increases in NE were observed in the ic veratrine animals with clamped adrenals. No significant increases in VO2 or catecholamine concentrations were observed after ic saline or iv veratrine administration. These data suggest that the elevated VO2 may have been mediated by adrenal catecholamines and that an increased metabolic rate may complicate the ability of patients with severe NPE to balance O2 supply with demand.

Adrenal Glands↗
PubMed1986

The sympathetic nervous system in essential hypertension.

Enhanced activity of the sympathetic nervous system (SNS) could contribute to essential hypertension (EH). Results of over 80 studies measuring norepinephrine (NE) in EH patients show that only a minority of younger EH patients have elevated plasma NE. Younger EH patients also have increased renal NE spillover and elevated 24-hour NE levels. Another method to evaluate SNS in EH patients is examination of depressor responses to SNS blocking agents. The level of plasma NE predicts the degree of depressor response after acute clonidine administration in EH patients, suggesting increased SNS outflow in EH. Stimulation of SNS activity by stress, isometric exercise, or tilt table shows exaggerated NE responses in EH patients and young normotensive individuals from hypertensive-prone families. EH patients with high plasma NE tend to be younger, thinner, have higher pulse rates, greater cardiac indices, accentuated depressor responses to SNS inhibition, and blunted baroreflex sensitivity. Patients with EH also display enhanced vascular reactivity to infused NE despite high plasma NE, which should normally blunt vascular reactivity. Baroreceptors modulate blood pressure increases through central inhibition of SNS outflow. EH patients display diminished baroreceptor control early in the development of EH, as seen in younger patients with borderline or mild EH. However, most evidence indicates that baroreflex abnormalities in EH are a secondary event. Elevations of plasma epinephrine (E) are also seen in EH. Stress in EH subjects causes increases in plasma E, accompanied by sodium retention and enhanced vascular reactivity. Stress-induced increases in plasma E may result in prejunctional uptake of E in nerve terminals with release of E as a cotransmitter with NE--i.e., facilitation of NE release leading to postjunctional vasoconstriction and hypertension. Another catecholamine product of SNS activity, dopamine (DA), may contribute to EH by its effects on aldosterone and sodium excretion. DA inhibits aldosterone secretion and enhances sodium excretion. Studies in EH patients show reduced urinary-free DA responses to salt loading. This suggests an intrinsic deficiency of DA-modulated natriuretic mechanisms in EH.

Antihypertensive Agents↗