[The sympathetic nervous system and balneotherapy].
Explore the source record for details and available documents.
Balneology↗
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.
CLINICO-PATHOLOGICAL conference: neuroblastoma arising from the abdominal sympathetic nervous system with metastases.
Explore the source record for details and available documents.
Neoplasms↗
[Experimental studies on the effect of sympathetic nervous system on cochlear function].
Explore the source record for details and available documents.
Cochlea↗
The sympathetic nervous system contributes to capsaicin-evoked mechanical allodynia but not pinprick hyperalgesia in humans.
The contribution of the sympathetic nervous system (SNS) to pain, mechanical allodynia (MA), and hyperalgesia in humans is controversial. A clearer understanding is crucial to guide therapeutic use of sympatholytic surgery, blocks, and drug treatments. In rats, capsaicin-evoked MA, and to some extent, pinprick hyperalgesia (PPH), can be blocked with alpha-adrenoreceptor antagonists. In this study, we examined the contribution of the SNS to MA and PPH in normal human subjects by blocking alpha-adrenoreceptors with intravenous phentolamine. In a double-blinded, placebo-controlled, crossover study, subjects were given IV saline or phentolamine, 1 mg/kg over 20 min. Ten minutes after the start of the infusion, subjects received 100 micrograms of intradermal capsaicin on the foot dorsum with the temperature of the injected site clamped at 36 degrees C. The temperature of the uninjected foot was used to monitor the degree of alpha-adrenoreceptor blockade produced by phentolamine. Ongoing pain and MA and PPH areas were measured every 5 min for 60 min. A significantly greater increase in temperature on the uninjected foot was seen during the phentolamine infusion compared with the saline infusion, indicating alpha-adrenergic blockade. Significantly less MA was observed with the phentolamine infusion 10-25 min after capsaicin injection than with the saline infusion. No significant differences in ongoing pain or PPH areas were seen between the two infusions at any time. Our results suggest that capsaicin-evoked MA and PPH have different mechanisms, with the SNS having a role in MA but not in PPH or ongoing pain.
Capsaicin↗
Role of angiotensin II in sympathetic nervous system induced left ventricular dysfunction.
Experiments were undertaken to determine whether angiotensin (Ang) II concentration increases during massive sympathetic nervous system (SNS) activation and whether such an increase plays a role in the pathogenesis of SNS-induced left ventricular (LV) dysfunction. We also sought to determine whether excessive Ca2+ uptake through L-type channels due to intense adrenoceptor activation is responsible for the LV dysfunction. AngII concentration was measured in the plasma and myocardium before and after massively activating the SNS with an intracisternal injection of veratrine. In separate experiments, rabbits were given losartan, enalaprilat, enalaprilat plus HOE-140, nifedipine, -Bay K 4866, or saline before massively activating the SNS. LV function was evaluated 2.5 h later. The intense SNS activity caused plasma and myocardial AngII to increase by 400 and 437%, respectively. AngII receptor blockade did not prevent LV dysfunction. In contrast, enalaprilat reduced the degree of dysfunction, but its cardioprotection was abolished by HOE-140. Although nifedipine prevented SNS-induced LV dysfunction, administration of the Ca2+ channel opener, -Bay K 4866, did not increase its severity. Our results indicate that AngII is not involved in the pathogenesis of SNS-induced LV dysfunction and that the cardioprotection provided by angiotensin converting enzyme (ACE) inhibition is due to activation of a bradykinin pathway. Furthermore, the finding that the magnitude of the LV dysfunction was reduced by enalaprilat, and not increased by -Bay K 4866, suggests that intense adrenoceptor activation of L-type Ca2+ channels is not the primary pathogenetic mechanism.
Adrenergic beta-Antagonists↗
Gender differences in fat oxidation and sympathetic nervous system activity at rest and during submaximal exercise in older individuals.
1. Gender differences in fat oxidation at rest and during exercise may contribute to higher body fat in women. We examined gender differences in fat oxidation at rest and during submaximal exercise and their relationship to sympathetic nervous system activity, free fatty acid availability, body composition and aerobic capacity in older volunteers. 2. We measured free fatty acid kinetics using [14C]palmitate, absolute (micromol/min) and relative (respiratory quotient) rates of fat oxidation by indirect calorimetry and sympathetic nervous system activity from noradrenaline kinetics using [3H]noradrenaline in 12 older men (70+/-4 years) and 12 older women (66+/-4 years) at rest and during 30 min of submaximal exercise (45% of peak oxygen consumption). 3. At rest, men oxidized more fat than women on both an absolute (88+/-19 versus 51+/-15 micromol/min; P<0.01) and relative (respiratory quotient: 0.80+/-0. 04 versus 0.85+/-0.04; P<0.01) basis. These differences were not related to noradrenaline appearance rate, free fatty acid concentration, body composition or aerobic capacity. During exercise, fat oxidation was higher (P<0.05 to P<0.01) in men on an absolute level, but respiratory quotient did not differ. Higher absolute fat oxidation in men during exercise was explained by their higher absolute workload. Plasma free fatty acids and free fatty acid rate of appearance did not differ between men and women during exercise despite higher (P<0.05 to P<0.01) plasma noradrenaline concentrations in men. 4. We conclude that: (i) resting fat oxidation is higher in older men compared with older women independent of differences in noradrenaline appearance rate, free fatty acid availability, body composition or aerobic capacity, and (ii) despite higher plasma noradrenaline concentrations during submaximal exercise, no gender differences in free fatty acid appearance rate or fat oxidation were found. These results suggest a sex dimorphism in post-absorptive fat metabolism in the elderly.
Aged↗
Sympathetic nervous system activity in rat thyroid: potential role in goitrogenesis.
The role of sympathetic innervation in regulation of thyroid function is incompletely understood. We, therefore, carried out studies in rats utilizing techniques of norepinephrine turnover to assess thyroid sympathetic activity in vivo. Thyroidal sympathetic activity was increased 95% by exposure to cold (4 degrees C), 42% by chronic ingestion of an iodine-deficient diet, and 32% in rats fed a goitrogenic diet (low-iodine diet supplemented with propylthiouracil). In addition, fasting for 2 days reduced sympathetic nervous system activity in thyroid by 38%. Thyroid growth and 125I uptake were also compared in intact and decentralized hemithyroids obtained from animals subjected to unilateral superior cervical ganglion decentralization. Unilateral superior cervical ganglion decentralization led to a reduction in thyroid weight, in 125I uptake by thyroid tissue, and in TSH-induced stimulation of 125I uptake in decentralized hemithyroids. These results suggest that sympathetic activity in thyroid contributes to gland enlargement and may modulate tissue responsiveness to TSH.
Animals↗
Sympathetic nervous system mediated cardiovascular effects of cocaine are primarily due to a peripheral site of action of the drug.
Currently, augmentation of sympathetic nervous system function produced by cocaine is thought to be due primarily to stimulation of sympathetic centers in the brain (central effect) and to inhibition of catecholamine uptake into postganglionic sympathetic nerve terminals (peripheral effect). In this review of our work, we present the following evidence that cocaine-induced changes in cardiovascular function, particularly those that peak within 1 to 5 min after an i.v. bolus injection of the drug, are due to a peripheral effect of the drug: (1) In both dogs and cats, cocaine potentiates the tachycardiac effect of neurally-released and injected norepinephrine (NE). The time course of action and dosage range of cocaine that produces potentiation follows that which increases blood pressure (BP), heart rate (HR), rate-pressure product and coronary vasoconstriction. (2) Cocaine given in i.v. doses that increase BP in decerebrate cats (0.25-1.0 mg/kg) has no significant effect on directly monitored spontaneous cardiac sympathetic nerve activity (SNA). In fact, higher doses of cocaine (2-4 mg/kg, i.v.) consistently inhibit preganglionic cardiac and splanchnic nerve activity. (3) Cocaine (0.1-1.0 mg) administered directly into the blood supply of the hindbrain via the vertebral artery produces no increase in BP, HR or SNA in cats; instead, decreases in BP and sympathetic activity occur. The same dose (1 mg), injected i.v., does not depress BP or SNA. In addition, cocaine injected into the forebrain via the carotid artery or into the cerebral ventricles (0.1-1.0 mg) has very little effect on BP. Our results indicate that there is no significant excitatory effect of cocaine on CNS sympathetic centers, and that the sympathomimetic effects of cocaine on the cardiovascular system are likely to be mediated at peripheral sites.
Animals↗
Hyperreactivity of the central sympathetic nervous system in vibration-induced white finger.
Vibration exposed workers with and without vibration-induced white finger (VWF), subjects with primary Raynaud's phenomenon and non-exposed controls were investigated in the present studies. The applied stimuli comprised cold stimuli, vibration exposure, and postural stimuli. The digital vasomotor responses to these stimuli were objectively quantified by measurements of finger systolic blood pressure and relative capillary blood flow rate in the skin of the finger. The results indicate that hyperreactivity of the central sympathetic nervous system may function as an/the abnormal element of the reflex mechanisms triggering the predominant portion of the vasoconstriction in episodic arterial closure of VWF. The hyperreactivity of the central sympathetic nervous system may be induced by prolonged exposure to hand-arm vibration, possibly by activation of the vibration elicited central sympathetic vasoconstrictor reflex mechanisms.
Adult↗
Urinary sodium excretion: association with hyperinsulinaemia, hypertension and sympathetic nervous system activity in obese and control children.
UNLABELLED: The aim of the present study was to evaluate the association between 24 h urinary excretion of sodium and blood pressure, fasting plasma insulin, renin, aldosterone and serum norepinephrine concentrations in 45 obese and 15 control children. Urinary sodium excretion was significantly lower in obese subjects (1.3 +/- 0.6 mmol/kg/24 h, P < 0.01) than in controls (2.8 +/- 1.3 mmol/kg/24 h). Hyperinsulinaemia did not affect sodium excretion of obese children. Plasma renin and aldosterone levels did not correlate with sodium excretion and were significantly higher in overweight children. Serum norepinephrine levels were also significantly higher in the obese group (0.66 +/- 0.89 microgram/100 ml) as compared to the controls (0.11 +/- 0.03 microgram/100 ml, P < 0.01) and showed significant negative correlation with urinary sodium excretion (r = 0.43, P < 0.05). CONCLUSION: Hyperinsulinaemia and the consequently increased sympathetic nervous system activity might be involved in the development of high blood pressure in obese children by decreasing urinary sodium excretion.
Adolescent↗
Transient hypogonadotrophic hypogonadism after head trauma: effects on steroid precursors and correlation with sympathetic nervous system activity.
Transient hypogonadotrophic hypogonadism commonly occurs after major medical insults. Because data on testosterone precursors are sparse and because little is known about the aetiology of these changes, we studied the interactions of traumatic brain injury with gonadal steroidogenesis and with sympathetic nervous system activation. Patients were divided into two groups based upon the severity of neurological dysfunction using the Glasgow Coma Score (GCS); Group 1 less than 8, Group 2 greater than or equal to 8. Group 1 was further divided into those patients treated (Group 1b) and those not treated with dexamethasone (Group 1a). Plasma levels of testosterone, androstenedione, 17-hydroxyprogesterone, DHEA sulphate, cortisol, LH, FSH, and the catecholamines noradrenaline (NE), adrenaline (EPI) and dopamine were measured in 31 acutely brain injured men, aged 18-95, shortly after their accident and 4 days later. In all patients, NE and EPI were elevated on admission (NE: 841 +/- 105 (SEM) pg/ml; EPI: 191 +/- 32 pg/ml and there were highly significant inverse correlations between admission NE (r = -0.52, P less than 0.003) and EPI (r = 0.44, P less than 0.02) levels and day 4 testosterone concentrations. Testosterone fell 53% (P less than 0.001) in 13 Group 1a men, but only 25% (P = NS) in the less severely injured. Similar reductions occurred in cortisol and the steroid precursors. However, only testosterone, 17-hydroxyprogesterone, and DHEA sulphate levels were significantly lower than normal on day 4. LH and FSH levels were also significantly reduced from elevated admission levels. In the eight men treated with dexamethasone (8-40 mg/ml) (Group 1b), the decrease in testosterone, LH and FSH concentrations were similar to those present in Group 1a. Thus, severe traumatic brain injury leads to hypogonadotrophic hypogonadism which affects testosterone and its precursors. The magnitude of the hormonal dysfunction is dependent upon the severity of the neurological insult. Finally, the decrease in testosterone is significantly correlated with admission catecholamine levels, which may suggest a role for the sympathetic nervous system (SNS) in mediating this response in men.
Adolescent↗
Sympathetic nervous system development in hypertensive rats.
The functional development of cardiac and adrenal medullary responses to reflex activation of the sympathetic nervous system was studied in preweanling spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rat pups. Pups from the two strains received injections of insulin or saline at 2, 4, 8, 12 or 16 days of age and were killed 3 h later. The induction of ornithine decarboxylase (ODC) in the heart and the depletion of epinephrine (EPI) from the adrenal medulla served as tissue markers of functional sympathetic neurotransmission. Compared with WKY pups, SHR pups showed a greater induction of ODC activity in the heart at 2, 4, and 8 days of age. There were no differences between SHR and WKY pups in the adrenal medullary response to insulin-induced hypoglycaemia. These altered patterns of sympathetic-target tissue development in early life may contribute to the higher arterial pressures maintained by SHR throughout life.
Adrenal Medulla↗
Obesity and hypertension: roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms.
Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remains to be determined.
Animals↗
Central administration of a nitric oxide synthase inhibitor causes pressor responses via the sympathetic nervous system and the renin-angiotensin system in Wistar rats.
The central roles of nitric oxide (NO) in regulations of the blood pressure and heart rate were examined in anesthetized rats. Intracerebroventricular (i.c.v.) injection of Nomega-nitro-L-arginine methyl ester (L-NAME) caused dose-dependent increase in the blood pressure and heart rate. The pressor response of the blood pressure to L-NAME (2 micromol, i.c.v.) was reduced by L-arginine (5 micromol, i.c.v). Pretreatment with a ganglionic blocker, pentolinium (10 mg/kg, i.v.), significantly inhibited both pressor responses induced by L-NAME (2 micromol, i.c.v). The later pressor response of the blood pressure to L-NAME was also inhibited by the angiotensin II AT-1 blocker losartan (10 mg/kg, i.v). These results suggest that the response of the blood pressure to L-NAME is mediated by both the sympathetic nervous system and the renin-angiotensin system.
Animals↗
Sympathetic nervous system involvement in the syndrome of painful legs and moving toes.
The objective of this study is to investigate sympathetic nervous system involvement in 2 patients with painful legs and moving toes. The first case was studied several years after the initiating trauma produced a peripheral nerve lesion and demonstrated the characteristic sequence of progression of pain and moving toes from the injured leg to the contralateral leg. The second case was initially studied within 3 months of an injury that did not produce definitive signs of a peripheral nerve lesion. Pain increased when the patients were startled and subsided temporarily after sympathetic blockade. In the first patient, toe movements and allodynia to light tactile stimulation persisted during sympathetic blockade, and pain sometimes returned before the vascular effects of blockade disappeared. In the second patient, pain and toe movements could be provoked reproducibly by light tactile stimulation of the affected foot and by sympathetic arousal. These symptoms and signs disappeared after lumbar sympathectomy, and re-emerged when signs of sympathetic reinnervation were detected. We concluded that sympathetic neuronal discharge may provoke pain by activating an impulse generator in the affected limb. Sympathetic involvement in the painful legs and moving toes syndrome appeared to be greater in the second case than the first, presumably due to differences in the initial injury or stage of the condition.
Adult↗
Gender differences in sympathetic nervous system regulation.
1. Females are protected against the development of hypertension. The purpose of the current review is to present the evidence for gender differences in the regulation of the sympatho-adrenal nervous system and to determine if these differences support the hypothesis that, in females, the regulation of the sympathetic nervous system (SNS) is altered such that sympatho-adrenal activation is attenuated or sympatho-adrenal inhibition is augmented. 2. The central control of sympatho-adrenal function is different in females and responses vary during the oestral and menstrual cycles. Pathways regulating the SNS appear to be less sensitive to excitatory stimuli and more sensitive to inhibitory stimuli in females compared with males. 3. Gender differences in arterial baroreflex sensitivity suggest that females may have a greater baroreflex sensitivity, such that alterations in blood pressure are more efficiently controlled than in males. Cardiopulmonary reflex inhibition of sympathetic nerve activity is greater in females, possibly resulting in a greater renal excretory function. 4. An attenuated sensitivity to adrenergic nerve stimulation, but not to noradrenaline (NA), suggests that gender differences in noradrenergic neurotransmission may protect females against sympathetic hyperactivity. Gender differences in the regulation of NA release via presynaptic alpha 2-adrenoceptors, the vasoconstrictor response to the cotransmitter neuropeptide Y and the clearance of catecholamines are consistent with this hypothesis. 5. Similarly, attenuated stress-induced increases in plasma catecholamines in women suggest that females are less sensitive and/or less responsive to adrenal medullary activation. This is supported by findings of gender differences in adrenal medullary catecholamine content, release and degradation. 6. We conclude that there is strong evidence that supports the hypothesis that, in females, the regulation of the SNS is altered such that sympatho-adrenal activation is attenuated or sympatho-adrenal inhibition is augmented.
Adrenal Medulla↗
Contribution of the sympathetic nervous system on the burn-associated impairment of CCL3 production.
Previously, we have reported that the susceptibility of burned patients to infectious complications is increased when the production of CC-chemokine ligand 3 (CCL3) is impaired. In this study, the role of the sympathetic nervous system on impaired CCL3 production and antibacterial resistance following burn injuries was investigated. Normal mice were resistant (65% survival) to cecal ligation and puncture (CLP)-induced sepsis, while the same CLP killed 90% of thermally injured mice (TI-mice). However, TI-mice resisted CLP-induced sepsis (60% survival) when they were previously treated with CCL3 or sympathectomized with 6-hydroxydopamine (6-OHDA). Augmentation of host resistance against CLP-induced sepsis by 6-OHDA was abrogated by anti-CCL3 mAb treatment. Norepinephrine (NE) production was increased in circulation of TI-mice, and treatment of TI-mice with 6-OHDA resulted in the inhibition of NE secretion. CCL3 production was impaired in cultures of T cells from TI-mice or normal T cells treated with NE, even when stimulated with anti-CD3 mAb. However, CCL3 was produced by mAb-stimulated T cells from TI-mice previously treated with 6-OHDA. These results indicated that by inhibiting CCL3 production the sympathetic nervous system contributes to the increased susceptibility of TI-mice to sepsis.
Animals↗
[ON THE ROLE OF THE SYMPATHETIC NERVOUS SYSTEM IN THE RESTORATION OF FUNCTION OF A REIMPLANTED LIMB IN DOGS].
Explore the source record for details and available documents.
Animals↗