[Effects of the sympathetic nervous system on the circulation of lymph in the limbs: experimental research by means of thorotrast lymphography].
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Extremities↗
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Results for “Sympathetic Nervous System”
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The role of the abdominal sympathetic nervous system in regulating portal venous flow and its functional distribution.
The role of the abdominal sympathetic nervous system in regulating portal venous flow (PVF) was examined in anesthetized rats using an ultrasonic volume flowmeter. Electrical stimulation of the hepatic sympathetic branch, given at 10 Hz, 1 ms, 10 s and 12 V, caused approximately a 28 percent reduction in PVF, which was equivalent to that produced by occlusion of the bilateral carotid arteries for 30 s, without causing any change in the systemic arterial pressure. Stimulation of the major splanchnic nerve decreased PVF, the response being greater by stimulation of the right nerve than by stimulation of the left (p less than 0.05). Bilateral adrenalectomy shortened the recovery time without changing the magnitude or lateral predominancy. Neither proper hepatic arterial occlusion nor partial hepatectomy affected the response. In the partially hepatectomized animals, stimulation of the hepatic branch did not decrease the splenic flow but decreased the superior mesenteric venous flow (SMVF) and induced a similar response in PVF even when the SMVF was interrupted. An intraportal injection of noradrenaline decreased PVF dose-dependently. These findings indicate that the sympathetic nerve regulates PVF directly, and that there is functional laterality of the regulatory mechanism in the abdominal cavity, which suggests that adrenal factors work together with the nerve that supplies the portal vein.
Adrenalectomy↗
Stimulatory influence of D(-)3-hydroxybutyrate feeding on sympathetic nervous system activity in the rat.
To examine the effect of ketone body utilization on sympathetic nervous system (SNS) activity, norepinephrine (NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of rats fed diets enriched with D(-)3-hydroxybutyrate (3OHB), the naturally occurring isomer of hydroxybutyrate. Isoenergetic substitution of 3OHB for chow for 4 days increased cardiac [3H]NE turnover (P < .025), with a slightly less marked (P < .06) effect in IBAT. When [3H]NE turnover was measured in rats fed chow diets supplemented with 3OHB or sucrose and compared with that in animals fed chow alone, [3H]NE turnover rates in heart and IBAT were similar in the ketone-supplemented and chow-fed groups. Animals fed the sucrose-supplemented chow displayed lower rates of [3H]NE turnover in IBAT than rates found in those given the 3OHB-containing chow (-36%, P < .025 in IBAT). In addition, the stimulatory effect on SNS activity of a 4-day exposure to a sucrose-enriched diet after 2 days of fasting was significantly enhanced by concomitant ketone ingestion. Fractional NE turnover in IBAT was increased from 9.3% +/- 1.3%/h in control rats to 14.2% +/- 0.9%/h in rats refed with 3OHB (P < .005). These observations indicate that increased ketone body utilization does not suppress SNS activity and may stimulate it in a manner quantitatively similar to that seen with carbohydrate or fat ingestion.
3-Hydroxybutyric Acid↗
The hyperactive child syndrome: peripheral sympathetic nervous system function and the effect of d-amphetamine.
We evaluated sympathetic nervous system function in medication-free hyperactive children by measuring plasma levels of norepinephrine (NE) and dopamine-beta-hydroxylase and then comparing the effects of two therapeutics doses of d-amphetamine to placebo in these patients. The medication-free hyperactive patients and controls had similar plasma NE levels and blood pressures while recumbent, and a similar increase in NE on standing, but the patients had a larger pressor response on standing. In the hyperactive patients d-amphetamine significantly increased blood pressure, pulse rate, and NE levels. The change in NE levels correlated with the change in amphetamine levels. The medication-free patients, when more anxious, had higher plasma NE levels.
Attention Deficit Disorder with Hyperactivity↗
Role of the sympathetic nervous system in peptic ulcer production in rats.
The role of the sympathetic nervous system in gastric acid secretion and in experimental duodenal ulceration (cysteamine induced) was studied in rats. The animals were divided randomly into seven groups: (1) control, (2) sham-operated, (3) surgical sympathectomy, (4) chemical sympathectomy (6-HODA), (5) vagotomy, (6) surgical sympathectomy plus vagotomy, and (7) chemical sympathectomy plus vagotomy. Results on gastric acid secretion were expressed as gastric acid output (GAO = micronEq of acid secretion in 1 hour). The means in the control and sham groups were 447.83 +/- 26.67 GAO and 399 +/- 36.4 GAO, respectively. The means in the sympathectomized rats (surgically = 562 +/- 27.21 GAO and chemically = 648.66 +/- 46.53 GAO) were higher (P less than 0.01) than those of the control and sham groups. In the vagotomized group the mean was 156.6 +/- 17.64 GAO, lower than those of the control and sham groups (P less than 0.001). The incidence of ulceration was 47.5% and 46% in the control and sham groups, respectively. Both the sympathectomized groups (surgically, 73%; chemically, 77%), had a significantly elevated incidence of ulceration as compared with the controls (P less than 0.01). The vagotomized group had a 14% incidence of ulceration. These results clearly indicate that sympathectomy has a definite effect on gastric acid secretion and on the incidence of experimental peptic ulceration in rats.
Adrenergic Fibers↗
Hypertension and insulin resistance: role of sympathetic nervous system activity.
The purpose of this study was to test the hypothesis that heightened sympathetic nervous system (SNS) activity contributes to the mechanism by which hypertension is associated with insulin resistance in humans. We performed frequently sampled intravenous glucose tolerance tests to determine tissue sensitivity to metabolic effects of insulin (SI) and measured plasma norepinephrine (NE) levels in 21 normotensive and 14 hypertensive Caucasian subjects. Compared with the normotensive subjects, hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x 10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels (normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23). In a multiple regression model, only body mass index (BMI) and mean arterial blood pressure (MABP) were significant independent predictors of SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001]; age, plasma glucose, epinephrine, and NE level did not enter this model. As an additional test of this hypothesis, seven hypertensive subjects were restudied after 10 days of guanadrel therapy to determine whether SI would increase during suppression of SNS activity by guanadrel. Despite a significant reduction in plasma NE levels with guanadrel (baseline: 1.63 +/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/- 0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude that, in the Caucasian population we studied, heightened SNS activity is not essential for the insulin resistance observed in hypertensive humans.
Adult↗
Association between low birthweight and high resting pulse in adult life: is the sympathetic nervous system involved in programming the insulin resistance syndrome?
To test the hypothesis that elevated sympathetic nervous system (SNS) activity could be determined in utero and be one of the processes mediating the link between size at birth and insulin resistance and raised blood pressure in adult life, we have studied the resting pulse rate of 449 men and women aged 46 to 54 (mean 50) years born in Preston, Lancashire, England whose birth size was recorded in detail. The subjects were visited at home by trained fieldworkers who measured resting pulse rate and blood pressure using an automated recorder. The resting pulse rate ranged from 44 to 108 (mean 73) beats min(-1). It rose with increasing body mass index (r = 0.14, p = 0.003) and waist to hip ratio (adjusted for sex r = 0.10, p = 0.003) and correlated significantly with systolic and diastolic blood pressures (p = 0.001), fasting glucose (p = 0.02), split proinsulin (p = 0.001), and triglyceride concentrations (p = 0.02). The pulse rate fell progressively from 76 beats min(-1) among subjects who weighed 5.5 lb (2.5 kg) or less at birth to 71 beats min(-1) among those who weighed 7.5 lb (3.3 kg) or more (decline in pulse rate per kg increase in birthweight = 2.7, 95 % CI 0.6 to 4.8 beats min(-1). The association was independent of current body mass index, waist to hip ratio and of potential confounding variables including smoking, alcohol consumption, and social class. Although the resting pulse rate is an imperfect index of SNS activity, these findings are consistent with the hypothesis that elevated SNS activity established in utero is one mechanism linking small size at birth with the insulin resistance syndrome in adult life.
Adult↗
Sympathetic nervous system response to graded exercise: effect of beta-blockade.
This study compares the sympathetic nervous system response to graded exercise in normotensive and essential hypertensive subjects with and without beta-adrenergic blockade. Blood pressure (BP), heart rate, and plasma norepinephrine (NE), epinephrine (E), and dopamine (DA) were measured just before starting the exercise (Pre-Ex), in the submaximal exercise (Sub-max),and after 8 minutes rest (Post-Ex). On placebo, Sub-max induced in both normotensives and hypertensives a similar increase in NE and E plasma levels. Plasma DA remained unchanged. Propranolol in controls and propranolol or mepindolol in hypertensives didn't modify significantly: 1) Pre-Ex plasma levels of E, NE, and DA; 2) response at Sub-max in controls; 3) plasma E and DA in hypertensive patients. In hypertensives on beta-blockade, submaximal exercise elicited a greater increase in plasma NE. Values for plasma NE in patients on propranolol were 1135 +/- 229 pg/ml higher than those obtained in the same patients on placebo (p less than 0.001). On mepindolol, the plasma NE increment was higher than that on placebo (p less than 0.05), but lower than that on propranolol (p less than 0.01). In controls, propranolol did not significantly modify BP at Pre-Ex or its response to exercise, whereas systolic and diastolic BP were significantly lower at Pre-Ex, Sub-max, and Post-Ex in hypertensives. On beta-blockade, heart rate decrease in Pre-Ex, Sub-max, and Post-Ex were not different in controls and hypertensives. The differences found on beta blockade would indicate that the effects of beta blockers are not identical in normotensive and hypertensive subjects.
Adrenergic beta-Antagonists↗
Increased sympathetic nervous system activity in rats fed a low-protein diet.
To examine the state of sympathetic nervous system (SNS) function in animals fed a protein-restricted diet, [3H] norepinephrine ([3H]-NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of rats fed synthetic diets of equal caloric density containing 22% protein (as casein) or 7% protein (the difference being made up by sucrose). Because dietary availability of tyrosine is a potential mediator of SNS responses to protein ingestion, a third diet (7% protein supplemented with tyrosine) was also tested. After 12 days dietary preparation [3H]-NE turnover was increased 35-70% in heart by 7% protein feeding and 93-103% in IBAT. When smaller animals were fed the synthetic diets for 4-5 wk, sympathetic stimulation in those given the protein-restricted formula was also apparent, although demonstration of this response was complicated by comparative problems due to the marked differences in body size between normal and protein-restricted groups. Addition of tyrosine (sufficient to normalize plasma and brain tyrosine levels) was without effect on the stimulation of NE turnover induced by the protein-deficient diet. Similarly, augmented urinary NE excretion observed in animals consuming the 7% protein diet was unaffected by supplemental tyrosine. Urinary dopamine excretion, however, was uniquely and strikingly elevated with restoration of dietary tyrosine to animals fed the low-protein diet. Thus isocaloric substitution of sucrose for casein in the diet activates the SNS in heart and IBAT, a response unrelated to limitation of dietary tyrosine.
Adipose Tissue, Brown↗
Reflex activation of sympathetic nervous system by ANF in humans.
Recent studies in experimental animal preparations suggest that ANF might alter sympathetic nervous system function. In the present investigation, direct recordings of postganglionic muscle sympathetic nerve activity were obtained from the peroneal nerve of conscious human volunteers. These data and hemodynamic parameters were recorded before and during infusions of atrial natriuretic factor (ANF, 99-126) or placebo (isotonic saline) in 10 subjects. Base-line ANF (36.5 +/- 3.8) increased to 329 +/- 22 pg/ml during 20-min infusions of ANF (15 ng.kg-1.min-1). This did not alter heart rate or blood pressure but reduced central venous pressure (CVP) by 47 +/- 10% (P less than 0.01). Base-line-integrated sympathetic activity (14.4 +/- 2.4 bursts/min) increased 30 +/- 12% during ANF infusion (P less than 0.05). However, when CVP was fixed at control levels with head-down tilt or lower body positive pressure, sympathetic activity was unchanged from pre-ANF base-line levels. These data indicate that exogenous infusions of ANF reduced CVP and unloaded cardiopulmonary baroreceptors. This elicits reflex increases of muscle sympathetic efferent activity. When CVP is maintained at control levels, ANF does not alter sympathetic neural outflow to muscles.
Atrial Natriuretic Factor↗
Sympathetic nervous system effects on feline bladder wall compliance throughout continence.
The urinary bladder is a compliant organ, high compliance being essential for useful urine storage. The extent to which the sympathetic nervous system promotes the storage of urine by increasing bladder compliance is unclear. The aim of the present study was to determine the range of bladder volumes over which the sympathetic nervous system increased bladder wall compliance. In supine, anaesthetized cats, the bladder was filled at twice the rate of natural filling, the continence cycle being interrupted at five stages. These stages were when the bladder had become globular, during prodromal contractions, soon after non-micturating contractions had commenced, approximately two-thirds of the way through the continence cycle and just prior to micturition. During each of these interruptions, bladder volume was held constant while pelvic nerve afferent activity and bladder pressure were recorded. Recordings were obtained before and during the intravenous infusion of trimethaphan, the resulting partial ganglion blockade decreasing arterial pressure by a third. Bladder pressure as well as afferent nerve activity increased significantly when the sympathetic drive was transiently blocked, indicating that there had been a prevailing net sympatho-inhibitory effect promoting bladder wall relaxation. This effect was observed during prodromal contractions and continued until the onset of micturition. This net sympatho-inhibitory effect is a potential therapeutic path for the treatment of bladder storage disorders.
Animals↗
Sympathetic nervous system as transmitter of mechanical loading in bone.
UNLABELLED: Sympathetic innervation has been demonstrated in bone. Adrenergic stimulation is one of the transmitters of bone loss by uncoupling between decreased bone formation and increased bone resorption. OBJECTIVE: By using a non-specific antagonist of -adrenergic pathway (propranolol per os), we hypothesized that we could rescue the uncoupling induced mechanical unloading bone loss in the rat model of tail-suspension. MATERIALS AND METHODS: Twenty-two female Wistar rats, 12 week-old, have been divided into three groups: eight tail-suspended rats (SR), six tail-suspended rats treated by propranolol (SRP) and eight non-suspended rats (NSR) during 30 days. Bone mineral density (BMD, g/cm2) has been measured by DXA (Hologic QDR-4500A) at D0 and D30 of the study, in the distal femoral metaphysis (DFM), the femoral diaphysis (FD), the whole body (WB, g) and body composition. RESULTS: Between D0 and D30, in DFM a significant variation in BMD is observed between NSR and SR (% BMD change: NSR +15.6 +/- 3.1% vs SR -1.0 +/- 1.4%, P < 0.0001) and BMD rescue in SRP group (% BMD change SRP +5.3 +/- 1.5% vs SR -1.0 +/- 1.4%, P = 0.03). In FD, gain of BMD is significant in NSR compared to SR (+17.5 +/- 1.5% vs +8.2 +/- 2.8%, P = 0.007) and to SRP (+17.5 +/- 1.5% vs +10.1 +/- 2.4%, P = 0.046). Gain in SRP group is not significant compared to SR group (P = 0.6). In WB, SRP gain more BMD than NSR (+14.0 +/- 1.8% vs +5.4 +/- 0.7%, P = 0.0002) and than SR (+14.0 +/- 1.8% vs +7.8 +/- 1.4%, P = 0.0043). There is no difference between NSR and SR groups (P = 0.19). CONCLUSION: We demonstrate that -adrenergic pathway of sympathetic nervous system is a major transmitter pathway of mechanical loading in rat bone. A specific study is necessary to analyse a possible systemic effect of propranolol in rat bone. Propranolol could be used to prevent the induced mechanical unloading bone loss as weightlessness
Absorptiometry, Photon↗
[Severe course of Wasiljew-Weil's disease with lesions of the sympathetic nervous system].
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Humans↗
[Research on the sympathetic nervous system. III. Differentiation of the effects of chemical mediators from the effects of sympathetic nerve excitation].
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Autonomic Pathways↗
Nephrectomy-induced alterations in the synthesis of catecholamines in the sympathetic nervous system and central nervous system.
Reduction in renal function is a key factor to the development of salt-dependent hypertension; however, the mechanism is obscure. To examine the role of the sympathetic nervous system (SNS) and central catecholaminergic neurons in this predisposition to the development of hypertension, the activity of tyrosine hydroxylase (TH) was determined in SNS and in several brain regions. In another group of unilaterally nephrectomized rabbits, cardiovascular responsiveness to norepinephrine was determined. A unilateral nephrectomy increased the activity of TH in the midmedulla, a brain region important in the baroreflex regulation of blood pressure, and in the adrenal gland, the major source of circulating catecholamines. The activity of TH was decreased in the pons-upper medulla region. No alterations were found in the proximal and distal mesenteric arteries, lower medulla, midbrain or hypothalamus. No alteration in blood pressure or cardiovascular responsiveness to norepinephrine was found. This study indicates that a unilateral nephrectomy produces long-lasting effects on central catecholaminergic neurons and the sympathetic nervous system without an effect on blood pressure or cardiovascular responsiveness.
Adrenal Glands↗
Plasticity of the sympathetic nervous system innervating the cerebral arteries in rats.
In order to investigate the neuroplasticity of the peripheral sympathetic nervous system innervating the cerebral blood vessels, we observed and traced the sprouting nerve fibers originating in the contralateral superior cervical ganglion (SCG) into the previously denervated cerebral arteries following unilateral excision of the SCG and/or decentralization of the contralateral SCG in young rats (4 weeks old). These nerve fibers were labeled anterogradely with wheat germ agglutinin-horseradish peroxidase or stained immunohistochemically with anti-tyrosine hydroxylase antibody. Eight weeks after the right SCG excision, reinnervating nerve fibers originating in the contralateral ganglion formed a circular pattern of nerve plexus only on the wall of the main cerebral arteries of the circle of Willis in the ganglionectomized side. However, the decentralization of the contralateral SCG, which was performed simultaneously with a unilateral SCG excision, prevented the nerve sprouting into the denervated regions. Unilateral decentralization of SCG itself failed to affect their distribution pattern or their density of nerve fibers originating in the ganglion. It is concluded that in the young rat the outgrowth of the sympathetic nerve fibers into the denervated cerebral arteries was strongly impeded by the disconnection of ganglion cells from the central nervous system, while the decentralization alone could not affect the innervation pattern of the postganglionic fibers which have been already built-up in the cerebral arterial system.
Animals↗
Interactions between angiotensin peptides and the sympathetic nervous system mediating intestinal sodium and water absorption in the rat.
The purpose of this study was to determine the locus of interaction of angiotensin peptides with the sympathetic nervous system leading to alterations in jejunal sodium and water transport. At low physiological doses, angiotensin II (AII) stimulates jejunal sodium and water absorption, while at high doses peptide inhibits absorption and/or stimulates secretion. Both the stimulation of jejunal transport and the inhibition of absorption were expressed in adrenalectomized rats. However, the stimulation of jejunal water absorption was abolished and a potentiated inhibition of transport was expressed in peripherally sympathectomized rats (intact adrenal medulla) and in normal rats after administration of guanethadine, phentolamine, and prazosin. The angiotensin analog (Sar1 Leu8)-AII has low efficacy and is a potent competitive antagonist of the parent peptide in pressor and myotropic systems, but is a full agonist with even greater potency than AII in stimulating jejunal transport. The increased water transport in response to (Sar1 Leu8)-AII is not secondary to enhanced renal renin release, as the analog also stimulated jejunal transport in the presence of captopril and after bilateral nephrectomy. The stimulation of absorption in response to (Sar1 Leu8)-AII alone or together with AII was abolished by phentolamine. These data demonstrate that AII-increased intestinal absorption is secondary to the release of norepinephrine from nerve endings in the jejunum and that AII inhibition of absorption is not mediated by the sympathetic nervous system. The analog (Sar1 Leu8)-AII is a full agonist in the stimulation of jejunal transport (increased norepinephrine release), but antagonizes the inhibitory response to high doses of AII. Angiotensin peptides are potent modulators of intestinal sodium and water absorption.
Adrenalectomy↗
Characteristics of the retrograde axonal transport system for nerve growth factor in the sympathetic nervous system.
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Animals↗