[Indirect therapy of certain dermatoses by irradiation of the sympathetic nervous system].
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Humans↗
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Results for “Sympathetic Nervous System”
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Neuromuscular dysfunction of the lower urinary tract with special reference to the influence of the sympathetic nervous system.
Filling cystometry, urethral and anal sphincter electromyography, pressure-flow registration, urethral closure pressure profile at rest and after alpha-adrenoceptor blockade with phentolamine, evoked potential of the bulbocavernosus reflex and denervation supersensitivity to carbachol in a-reflexic bladders were performed in 57 consecutive patients with a localized neurological lesion, in order to evaluate the relative importance of the somatic, the parasympathetic and especially the sympathetic nervous system for the function of the lower urinary tract. In spinal lesions with detrusor hyperreflexia, dyscoordination between detrusor and striated urethral sphincter was dominant, while in cauda equina lesions and in lesions of the pelvic nerves the lack of parasympathetic bladder innervation dominated. It was not possible to identify specific spinal segments controlling sympathetic nervous regulation of the lower urinary tract. The only influence of the sympathetic nervous system was a control of urethral pressure, where a statistically significant smaller proportion of the maximal urethral pressure was affected after alpha-adrenergic blockade in patients with peripheral nerve lesions. All a-reflexic bladders exhibited denervation supersensitivity to carbachol, while carbachol did not change urethral pressure significantly indicating minimal influence of the parasympathetic nervous system on urethral pressure.
Adolescent↗
Antihypertensive drugs and sympathetic nervous system.
Several studies have demonstrated that essential hypertension is accompanied by sympathetic activation, which contributes to blood pressure elevation. Sympathetic activation also has adverse consequences in hypertensive patients beyond initiating blood pressure elevation. There is evidence that neural vasoconstriction has metabolic effects in skeletal muscle, impairing glucose delivery to muscles. In the liver, retarding of post prandial clearance of lipids contributes to hyperlipidemia. Cardiac sympathetic activation is a probable cause of sudden death in hearth failure. A trophic effect of sympathetic activation on cardiovascular growth is also likely, contributing to the development of left ventricular hypertrophy. Consequently, one of the major aims of antihypertensive therapy should be to attenuate sympathetic tone. It is possible that, among the antihypertensive drugs available, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk.
Adrenergic alpha-Antagonists↗
Topical organization of the cardiac sympathetic nervous system.
A thorough understanding of the innervation pathways to the heart is requisite for studying the effects of the sympathetic nervous system. Knowledge of these pathways and how to selectively activate or eliminate them allows for the production of unique animal models for further investigation about the interaction between the cardiac sympathetics and the heart during ischemia.
Animals↗
Contribution of sympathetic nervous system activity during administration of carvedilol in rats with dilated cardiomyopathy.
We investigated the contribution of the sympathetic nervous system (SNS) in maintaining blood pressure during administration of carvedilol in rats with dilated cardiomyopathy, and examined whether SNS hyperactivity induced by high-dose carvedilol is related to severity of heart failure. The hypotensive effect of carvedilol in rats with heart failure (Group F) was not significantly different to that in rats without (Group N). However, enhancement of the plasma norepinephrine concentration during carvedilol administration in Group F was higher than in Group N. The constitutive plasma NE concentration in Group F (562 +/- 146 pg/ml) was significantly higher than in Group N (203 +/- 55 pg/ml) and there was a significant positive correlation between the heart weight to body weight ratio and the plasma norepinephrine concentration. Values for the maximal effect of the norepinephrine hypertensive effect during norepinephrine intravenous infusion (Emax) decreased, and plasma norepinephrine concentrations at half-maximal effect of the norepinephrine hypertensive effect (EC50) increased in Group F compared with Group N (20.8 +/- 6.1 and 28.6 +/- 2.2 mmHg, and 4.5 +/- 1.9 and 1.5 +/- 0.2 ng/ml, respectively). These results suggested that the number of receptors (Emax) and sensitivity (EC50) to the norepinephrine hypertensive effect decreased in Group F. Changes in these parameters in Group F corresponded with the results of a beta-adrenergic receptor binding assay using I-125 iodocyanopindolol (Bmax = 32 +/- 4 in Group F and 53 +/- 2 fmol/mg protein in Group N). These results showed that the SNS (presynaptic) activity increased and the SNS receptor sensitivity in the blood pressure regulation system decreased in heart failure. Therefore, high-dose carvedilol treatment should be used with caution to avoid worsening heart failure.
Animals↗
Developing renal innervation in the spontaneously hypertensive rat: evidence for a role of the sympathetic nervous system in renal damage.
The spontaneously hypertensive rat (SHR) exhibits increased renal sympathetic nerve activity and neurotransmitter levels compared with the control Wistar-Kyoto rat (WKY). These renal nerve abnormalities have been implicated as the cause of hypertension in the SHR. The aims of the present study were to characterize the ontogeny of renal sympathetic innervation in SHR in order to determine any functional implications. Glyoxylic acid histofluorescent and radio-enzymatic norepinephrine assays demonstrated an accelerated development of renal innervation in newborn and 1-, 2-, 3- and 6-week-old SHR compared with WKY. Sympathetic nervous system function was blocked in developing male SHR by treating pups from days 0 to 14 with: (1) guanethidine, (2) combined alpha- and beta-receptor antagonists (prazosin and timolol), or (3) vehicle (5% sucrose). Blood pressure (mean), renal function (plasma creatinine) and histologic renal damage were assessed at 42 weeks of age. Although the blood pressure of the drug-treated rats remained elevated, renal damage was reduced and renal function was improved compared with control (sucrose-treated) SHR. The data demonstrate that the SHR kidney develops a precocious sympathetic innervation and that inhibition of the development of sympathetic function ameliorates renal damage independently of systemic hypertension.
Animals↗
Role of the sympathetic nervous system in cold-induced hypertension in rats.
Hypertension develops in rats exposed chronically to cold [6 +/- 2 degrees C (SE)] and includes both an elevation of mean arterial pressure and cardiac hypertrophy. Previous studies suggest that cold-exposed animals, at least initially, have a large sustained increase in the activity of their sympathetic nervous system, suggesting a failure of the baroreceptor system to provide sufficient negative feedback to the central nervous system. The present study was designed to investigate whether alterations in the activity of the sympathetic nervous system, including the baroreceptor reflex, occur during exposure to cold and whether they contribute to cold-induced hypertension. Twenty male rats were prepared with indwelling catheters in the femoral artery and vein. Ten of the rats were exposed to cold (6 +/- 2 degrees C) chronically, while the remaining 10 were kept at 26 +/- 2 degrees C. Withdrawal of arterial blood samples (less than 5 ml/kg), measurement of direct arterial pressures, and measurement of baroreflex function were carried out at 0800 h at intervals throughout the experiment. Norepinephrine and epinephrine concentrations in plasma were also determined at intervals throughout the experiment. Systolic, diastolic, and mean blood pressures of cold-exposed rats were increased to levels significantly above those of controls. The sensitivity of the baroreflex (delta heart period/delta mean arterial pressure) was decreased in the cold-treated group. The concentration of norepinephrine in plasma increased after 24 h of exposure to cold and remained elevated throughout the experiment, whereas the concentration of epinephrine in plasma increased initially but returned to control levels after 19 days of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Pathophysiology of obesity-related hypertension: role of insulin and the sympathetic nervous system.
Reviewed herein are data supporting the hypothesis that insulin and the sympathoadrenal system are involved in the pathogenesis of hypertension in the obese. Data from the Normative Aging Study, a population-based cohort followed in Boston, confirm other epidemiologic reports of a direct relationship between upper-body obesity, hyperinsulinemia, and hypertension. Because insulin is known to stimulate the sympathetic nervous system (SNS), the possibility that insulin-mediated sympathetic stimulation contributed to hypertension in the obese was investigated by the analysis of 24-h urinary norepinephrine (NE) excretion in this group. Urinary NE was directly correlated with body mass index and waist/hip ratio, supporting increased SNS activity in the obese. Epinephrine excretion, an index of adrenal medullary activity, was inversely related to obesity, and both high insulin and low epinephrine levels were independently correlated with lower levels of high-density lipoprotein cholesterol and higher levels of triglycerides. These results are consistent with the hypothesis that insulin-mediated sympathetic stimulation results in hypertension from concomitant sympathetic stimulation of the heart, vessels, and kidney. Reciprocal changes in adrenal medullary function contribute to the associated dyslipidemia. Therapeutic strategies aimed at diminishing insulin resistance and lowering insulin levels, and antagonizing the effects of sympathetic stimulation on the heart, the vessels, and the kidneys, would appear to have a solid physiological rationale in the obese.
Animals↗
[The mechanism of the effect of the sympathetic nervous system on skin receptors].
It has been found that smooth muscles play an important role in the mechanism of a sympathetic nervous system effect on the activity of skin receptors. Greater activity of the sympathetic nerve fibres induces higher tension of smooth muscles and thus changes mechanical state of the tissues around the receptors. The latter condition, in its turn, affects the response of receptors to mechanical stimulation. A change in the smooth muscles tension in skin vessels affects the response of receptors to cooling of skin.
Afferent Pathways↗
Neurophysiological aspects of penile erection: the role of the sympathetic nervous system.
Recent studies have revealed that the initiation, maintenance and rigidity of penile erection are under parasympathetic and somatotopic control. The mechanism of penile detumescence is still under debate. Single and combined cavernous and hypogastric nerve stimulation was used to study the influence of the sympathetic nervous system on penile erection and to identify the mechanism of penile detumescence. Penile arterial flow and intracorporeal pressure recordings during various stimulation patterns indicated that erection induced by stimulation of the cavernous nerve could be blocked by excitation of the upper hypogastric nerves. Venous outflow studies demonstrated that the inhibitory effect of the sympathetic nervous system was due to active vaso- and corporeal smooth muscle constriction. It was concluded that subsidence and suppression of erection is a sympathetic function. Previous studies have shown that the neurophysiology of erection can be explained by 3 major inhibitory (sympathetic). Our findings are of clinical importance, since a better appreciation of the basic erectile mechanism is essential for successful management of erectile dysfunction.
Animals↗
Lack of relationship between sympathetic nervous system activity, measured by two circulating markers, and blood pressure in diabetic and nondiabetic subjects.
Two putative sympathetic nervous system (SNS) markers, noradrenaline and neuropeptide Y (NPY) were related to 24-h ambulatory blood pressure (BP) in 59 normotensive subjects, 34 non-insulin-dependent diabetics, and 25 controls. Plasma NPY levels were not significantly different between the two groups [non-insulin-dependent (NIDDM) diabetes mellitus 4.33 (3.25-5.78), controls 5.68 (3.39-6.97) p=0.26] as were those of noradrenaline (1.51+/-0.69 versus 1.78+/-0.55; p=0.053). There were correlations, controlled for age and obesity, of plasma NPY with clinic and night time diastolic BP in the control group only (r=0.49 [p=0.013] and r=0.48 [p=0.023] respectively). No similar correlation was found in the NIDDM group, or between plasma noradrenaline and blood pressure in either group. No correlation was found between plasma insulin and NPY or noradrenaline levels. There is a weak independent relationship between NPY and blood pressure in normotensive nondiabetics but not in NIDDM subjects. We found no evidence for the hypothesis that insulin modulates blood pressure through activity of the SNS.
Adult↗
[Research on the sympathetic nervous system. I. Adrenolytic beta-phenoxyisopropylamine induction of dissociation of the effects of noradrenalin & sympathetic stimulation of the cardiovascular system of the dog].
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Adrenergic Antagonists↗
Role of sympathetic nervous system in experimental hypertension and diabetes mellitus.
An investigation has been made to elucidate the role of sympathetic nervous system (SNS) in the development of renal hypertension and hyperglycemia in rats and rhesus monkeys using 6-hydroxydopamine (6-OHDA). Development of renal hypertension was blocked in weanling rats (80%), demedullated adult rats with 6-OHDA (75%) but not in adult rats sympathectomised with 6-OHDA. Weanling rats treated with 6-OHDA did not have any detectable catecholamine stores when measured 60 days after treatment with 6-OHDA. Unlike the weanling rats the hearts of the adult rats showed significant refilling of catecholamines 60 days after 6-OHDA treatment. 6-OHDA treatment and adrenalectomy did not modify the development of streptozotocin (STZ) induced hyperglycemia and the hypoglycemic effect of tolbutamide and phenformin. Chemical sympathectomy with 6-OHDA did not show any glucose intolerance in rhesus monkeys or any effect or insulin release. Phentolamine (PHE) and oxprenolol (OXP) pretreatment had no effect on development and maintenance of hyperglycemia. Although there was no effect on the endogenous catecholamines stored in the heart and brain in the diabetic rats, there was a marked increase in the urinary excretion of norepinephrine (NE), epinephrine (E), 3-methoxy-4 hydroxy mandelic acid (VMA) and creatinine. The rate of disappearance of (3H)-NE from rat heart was higher when compared to age matched controls. Diabetic rats showed increase responsiveness to angiotensin II and developed hypertension faster when their renal arteries were clamped as compared to controls. It is concluded that the functional SNS is important in the development of renal hypertension in the rat. Further the SNS in the rats and rhesus monkeys does not play any significant role in the STZ induced hyperglycemia, glucose intolerance and insulin release.
Adrenalectomy↗
Angiotensin II augments reflex activity of the sympathetic nervous system during cardiopulmonary resuscitation in pigs.
BACKGROUND: During hypotensive states, angiotensin II augments reflex activity of the sympathetic nervous system. The purpose of the present study was to assess the effects of this vasoconstrictor on myocardial blood flow and plasma catecholamine concentrations during and after CPR. METHODS AND RESULTS: After 4 minutes of ventricular fibrillation and 3 minutes of open-chest CPR, 14 pigs (24 to 26 kg) were randomized into two groups receiving either saline (n = 7) or 0.05 mg/kg angiotensin II (n = 7). Arterial plasma catecholamine concentration was measured with high-pressure liquid chromatography. Organ blood flow was measured with radiolabeled microspheres. During CPR, after drug administration, left ventricular myocardial blood flow was significantly higher in the angiotensin II-treated group than in the control group. During CPR, median epinephrine concentrations before and 90 seconds and 5 minutes after drug administration were 63.0, 35.2, and 22.5 ng/mL, respectively, in the control group and 63.2, 139.8, and 154.2 ng/mL, respectively, in the angiotensin II group (P < .001 at 90 seconds and P < .01 at 5 minutes). At the same times, median norepinephrine concentrations were 52.6, 59.8, and 33.9 ng/mL, respectively, in the control group and 42.5, 98.7, and 111.3 ng/mL, respectively, in the angiotensin II group (P < .01 at 5 minutes). Restoration of spontaneous circulation was possible in all of the angiotensin II-treated pigs, whereas only 3 of the 7 saline-treated pigs could be resuscitated. At 5 minutes after successful resuscitation, epinephrine was 6.8 ng/mL in the control group and 16.1 ng/mL in the angiotensin II group (P < .05). CONCLUSIONS: During CPR, angiotensin II appears to increase coronary perfusion pressure and myocardial blood flow, not only by direct peripheral arteriolar vasoconstriction via angiotensin II receptors but also by inducing a massive catecholamine release with adrenergic peripheral vasoconstriction.
Angiotensin II↗
Impact of sleep apnea on sympathetic nervous system activity in heart failure.
OBJECTIVES: To compare and establish the relevance of the relative degree of sympathetic nervous system activity (SNSA) in groups of patients with congestive heart failure (CHF) and obstructive sleep apnea (OSA), and in a control group. BACKGROUND: Elevated SNSA is a characteristic feature of CHF, as well as of OSA and nonhypercapnic central sleep apnea (CSA). OSA and CSA commonly occur with CHF; however, the relative contribution of apnea-related hypoxemia and sleep fragmentation to the SNSA of patients with CHF is not known. METHODS: This was a prospective, controlled, observational trial in which the overnight urinary norepinephrine (UNE) level, which is a measure of integrated overnight SNSA while asleep, was measured in 15 healthy male volunteers, 15 male OSA patients who did not have CHF, and 90 CHF patients (77 men). CHF patients also had right heart pressure measurements and then were grouped by the presence of sleep apnea. RESULTS: Compared with healthy individuals, the mean (+/- SD) UNE level was significantly elevated in the OSA group and was even further elevated in the CHF group (13.4 +/- 5.6 vs 19.7 +/- 12.3 vs 32.2 +/- 20.2 nmol/mmol creatinine, respectively; p < 0.001 [by analysis of variance]). Within the CHF group, the mean UNE levels were greatest in the CHF-CSA group compared with the CHF-OSA group and the CHF nonapnea group (43.9 +/- 24.1 vs 24.0 +/- 10.8 vs 22.4 +/- 8.9 nmol/mmol creatinine, respectively; p < 0.001). Using a multivariate regression model, the variance of the UNE level in the CHF group was predicted, in descending order, by pulmonary capillary wedge pressure (14% variance), rapid eye movement sleep (8%), and the mean sleep pulse oximetry level (7%). CONCLUSIONS: Overnight SNSA is significantly greater in CHF patients than in OSA patients. Moreover, the hemodynamic severity of CHF contributes to the elevation of SNSA in CHF patients to a greater degree than apnea-related hypoxemia.
Adult↗
[Effects of sympathetic nervous system stimulation on complement content of blood serum].
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Complement System Proteins↗
Central corticotropin-releasing hormone activates the sympathetic nervous system and reduces immune function: increased responsivity of the aged rat.
CRH acts within the brain to activate the sympathetic nervous system and reduce cellular immune function. To determine the effects of age on CRH-induced elevations of sympathetic activity and suppression of immunity, we examined the responses of plasma catecholamines, neuropeptide-Y (NPY), corticosterone, and splenic natural killer (NK) activity after microinjection of rat CRH (200 pmol) into the lateral ventricle of aged (24-month-old) Fischer 344 (F344) rats compared to those in young (4-month-old) F344 rats. Basal concentrations of plasma norepinephrine and NPY were higher in the aged than in the young animals. In addition, CRH produced a greater elevation of plasma levels of catecholamines and NPY, which persisted for a longer period of time in the aged rats compared to responses in the young animals. Splenic NK activity showed an age-related decrement at baseline, and CRH induced a further significant (P less than 0.01) reduction of lytic activity in the aged rats, but did not alter cytotoxicity in the young rats. Corticosterone basal levels and responses were similar in the aged and young rats. These results show an age-related increase in autonomic outflow and suppression of NK activity after central CRH administration. In aged animals, the central nervous system may have a role in abnormal regulation of sympathetic activity and suppression of natural cytotoxicity in vivo.
Aging↗
[Hyperthyroidism and the sympathetic nervous system].
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Humans↗