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PubMed1996

Effects of insulin on vascular tone and sympathetic nervous system in NIDDM.

Chronic activation of the sympathetic nervous system may be a pathogenetic mechanism by which hyperinsulinemia induces cardiovascular damage in insulin-resistant NIDDM patients. The influence of physiological hyperinsulinemia (approximately 700 pmol/l) on basal and stimulated sympathetic outflow was studied in 12 lean normotensive subjects with well-controlled NIDDM without complications and in 13 matched control subjects. Forearm blood flow (FBF) was measured with forearm plethysmography; sympathetic nervous system activity was assessed by the [3H]norepinephrine (NE) tracer method. NIDDM patients were insulin resistant (glucose infusion rates 31.8 +/- 3.8 vs. 48.7 +/- 2.0 mumol.kg-1.min-1 in control subjects, P < 0.01). After a mixed meal, NIDDM patients showed a hyperinsulinemic response (2-h insulin levels: NIDDM patients 324 +/- 34 pmol/l, control subjects 165 +/- 19 pmol/l, P < 0.001). Insulin infusion induced a vasodilator response (not significantly different between the groups). Arterial plasma NE levels and total-body NE spillover increased significantly (total spillover in NIDDM patients from 0.77 +/- 0.09 to 1.18 +/- 0.16 nmol.m-2.min-1, in control subjects from 0.98 +/- 0.14 to 1.23 +/- 0.18 nmol.m-2.min-1, P < 0.01 for all, not different between groups). Total-body NE clearance did not change. Sympathetic stimulation (lower-body negative pressure [LBNP] 15 mmHg) induced forearm vasoconstriction and increased arterial and venous plasma NE and total NE spillover. Responses of FBF and NE kinetics to LBNP were not significantly different between groups and were not altered by hyperinsulinemia. Although these nonobese subjects with uncomplicated NIDDM showed postprandial hyperinsulinemia and resistance to the effect of insulin on glucose metabolism, this group was not resistant to the vasodilator and sympathetic stimulant effects of insulin. Responses to sympathetic stimuli (LBNP) were normal and unaffected by physiological hyperinsulinemia. Therefore, because of daily life hyperinsulinemia, chronic sympathetic stimulation could be operative in these patients and may explain the increased incidence of hypertension and/or cardiovascular complications.

Adult↗
PubMed1985

The influence of the sympathetic nervous system on the development of beta-adrenergic receptors in the rat submandibular salivary gland.

During the development of the rat submandibular gland (SMG) there is a clearly-defined sequence in the maturation of the beta-adrenergic receptor/adenylate cyclase-linked stimulus-secretion coupling system. The sympathetic nervous system does not become functionally linked to the exocrine process in the SMG until approximately six days after birth. The temporal correlation of the ingrowth of catecholamine-containing nerve processes, the appearance of beta-adrenergic receptors and the functional coupling of the stimulus-secretion system suggested the possibility of a cause and effect relationship between the appearance of the catecholamine-containing nerves in the gland and the maturational increase in the number of beta-adrenergic receptors. Chemical sympathectomy in neonates did not effect the time of appearance or the number of beta-adrenergic receptors seen in the developing gland. However, chronic isoproterenol treatment resulted in accelerated maturation of the gland with a concomitant premature appearance of the beta-receptors. These data suggest that the increase in the number of beta-adrenergic receptors which normally occurs in the developing gland at 5-6 days after birth is a specifically-programmed step closely associated with the degree of maturation attained by the cells and is independent from the ingrowth of catecholamine-containing nerves.

Animals↗
PubMed2001

Short-term sertraline treatment suppresses sympathetic nervous system activity in healthy human subjects.

Increased sympathetic nervous system (SNS) activity has been associated with stress, major depression, aging, and several medical conditions. This study assessed the effect of the selective serotonin reuptake inhibitor (SSRI), sertraline, on sympathetic nervous system (SNS) activity in healthy subjects. Twelve healthy volunteers participated in a double-blind, placebo-controlled, norepinephrine (NE) kinetic study, in which the effects of sertraline on SNS activity were ascertained by determining NE plasma concentrations and NE plasma appearance rates and clearance rates in sertraline or placebo conditions. Subjects received 50 mg of sertraline or placebo for two days and then one week later underwent the same protocol with the other drug. By single compartmental analysis, plasma NE appearance rates were significantly lower in the sertraline compared to the placebo condition (0.26+/-0.10 vs 0.40+/-0.23 microg/m(2)/min; P=0.04). Our study found that the net effect of short-term SSRI treatment is an apparent suppression of SNS activity as indicated by a decreased plasma NE appearance rate in the sertraline condition. If this preliminary finding can be extended to long-term treatment of patients, this could have significant therapeutic relevance for treating depression in elderly patients or those with cardiac disease, in which elevated SNS activity may exacerbate underlying medical conditions.

Adult↗
PubMed1977

[Systemic arterial hypertension: pathogentic role of the sympathetic nervous system].

Role of the clinical and experimental data suggesting the role of the sympathetic nervous system in some essential hypertension are reviewed: increase in heart rate and diastolic blood pressure during orthostatism, increase in cardiac output resulting from increase in cardiopulmonary blood volume and/or in myocardial contractility, increase in peripheral resistances, elevated plasma catecholamines and dopamine-bêta-hydroxylase, disturbances in arterial baroreceptor sensitivity and in vascular response to adrenergic stimuli, elevated plasma renin activity. It appears that the role of a sympathetic overactivity is mainly important in labile hypertension with hyperkinetic syndrome and elevated plasma renin activity.

Animals↗
PubMed2002

Polymorphisms of genes encoding components of the sympathetic nervous system but not the renin-angiotensin system as risk factors for orthostatic hypotension.

OBJECTIVE: The genetic background of orthostatic hypotension, an important risk factor for future cardiovascular morbidity and mortality, was investigated. DESIGN AND METHODS: The study subjects comprised 415 community-dwelling individuals, who were free from any cardiovascular complications, aged 50 years or older (mean age 70.5 +/- 9 years). Basal systolic blood pressure (SBP) was measured twice in supine posture after resting for more than 10 min. The orthostatic change in SBP was determined at 1 min and 3 min after standing up. The maximum change in SBP after standing was determined. Orthostatic hypotension was defined as a decline in SBP greater than 20 mmHg. The polymorphisms of genes encoding components of the renin-angiotensin system and sympathetic nervous system, which play pivotal roles in postural change in blood pressure regulation, were determined. RESULTS: There were no significant associations between the maximum change in SBP, the prevalence of orthostatic hypotension and gene polymorphisms of angiotensin-converting enzyme I/D, angiotensinogen M235T and angiotensin II type 1 receptor A1166C. On the contrary, polymorphism of the Gs protein alpha-subunit (GNAS1) T131C was significantly associated with the maximum change in SBP after standing [1.9 +/- 16 versus -3.6 +/- 16 mmHg (TT + TC versus CC), P = 0.008]. The prevalence of orthostatic hypotension was significantly different among GNAS1 genotypes (chi squared = 10.12, P = 0.011) and G-protein beta 3 subunit (GNB3) genotypes (chi squared = 6.12, P = 0.020). Multiple logistic regression analysis showed that both GNAS1 CC genotype [odds ratio (OR) = 2.79, 95% confidence interval (CI) 1.35-5.79, P = 0.006] and GNB3 C allele (OR = 1.78, 95% CI 1.06-3.00, P = 0.030) were independent risks for orthostatic hypotension. CONCLUSIONS: These findings indicate that genes encoding sympathetic nervous components could be involved in the predisposition for orthostatic hypotension.

Aged↗
PubMed1979

[Morphology of experimental tumors of the sympathetic nervous system].

Morphology of experimental tumours of the sympathetic nervous system in rabbits and hamsters induced by administration of nitrose compounds and the use of modifying factors was studied. The tumours were localized in the mediastinum, retroperitoneal space, adrenals and kidneys. The predominant involvement of the female animals was observed. Histological, histochemical and electron microscopic study of 33 tumours of the sympathetic nervous system was carried out. The tumours were classified as ganglioneuromas, ganglioneuroblastomas and sympathoblastomas by their degree of maturity. The experimental tumours by their structure were similar to the analogous neoplasias of man.

Adrenal Gland Neoplasms↗
PubMed1998

The sympathetic nervous system and ischaemic heart disease.

The sympathetic nervous system, coronary artery disease and myocardial ischaemia are related in different ways. First, the sympathetic system may be involved in the process of atherosclerosis through platelet activation and subsequent platelet-derived growth factor formation and by inducing mechanical injury to the vascular wall as a result of increased blood pressure and increased flow velocity. Secondly, sympathetic control of coronary vasomotor tone, which under normal conditions is not important, becomes functionally significant once coronary artery disease endothelial dysfunction has occurred. Under these circumstances, increased sympathetic adrenergic tone may lead to coronary vasoconstriction and, as myocardial oxygen demand increases concomitantly, myocardial ischaemia may ensue. Alternatively, myocardial ischaemia activates several neurohormonal systems, such as the sympathetic and, during more severe ischaemia, the circulating renin-angiotensin system. This leads to systemic and, possibly, coronary vasoconstriction and thus to further myocardial ischaemia. Prolonged myocardial ischaemia results in progressive norepinephrine release from the heart, reaching extracellular levels as high as 100-1000 x plasma concentrations. As cardiac beta-receptor density rises simultaneously, sympathetically-induced irreversible myocardial damage may occur, although through concomitantly increased beta-receptor kinase activity the beta-receptor may become functionally inactive. To counteract the detrimental effects of enhanced sympathetic activation on the heart, beta-blockade appears to be the proper choice. However, acute beta-blockade may lead to more profound ischaemia-induced neurohormonal activation and hence to vascular constriction through unoccupied alpha-receptors. In contrast, under ischaemic conditions and with concomitant beta-blockade, acute alpha-blockade does improve subendocardial flow and reduces myocardial ischaemia. A novel approach to anti-ischaemic therapy, which relates to modulating ischaemia-induced sympathetic activation, is through ACE inhibition. ACE inhibitors affect myocardial ischaemia by reducing neurohormonal activation and related systemic and coronary vasoconstriction. These acute effects may become more important over time, as coronary endothelial function improves following long-term ACE inhibition. A large multicentre controlled trial comparing ACE inhibition with placebo in patients with coronary artery disease, the EUROPA (EUopean trial on Reduction Of cardiac events with Perindopril in stable coronary Artery disease), which is currently underway, addresses the issue of whether ACE inhibition does in fact offer a novel approach in myocardial ischaemia.

Adrenergic alpha-Antagonists↗
PubMed1994

Unique problems in the treatment of the older hypertensive male. Introduction: increased sympathetic nervous system activity in the elderly.

Sympathetic activation increases blood pressure via effects on the heart, blood vessels and the kidney, and influences micturition and prostatic function via effects on the urinary sphincter and prostate muscular stroma. A systematic increase in sympathetic activity in older subjects would be expected to cause or exacerbate both hypertension and prostatism. Although assessment of sympathetic nervous system activity in humans is difficult, available evidence accumulated over the last decade strongly suggests that ageing is associated with increased sympathetic nervous system activity. There is general agreement that plasma norepinephrine levels are elevated in old, as compared with young, healthy human subjects. Furthermore, the rate of entry of norepinephrine into the circulation, a measure of sympathetic activity, is increased in older subjects. Plasma norepinephrine responses to both cardiovascular and metabolic stimuli are also accentuated in the aged so that the rise in plasma norepinephrine with upright posture and in response to oral glucose ingestion is greater in old than in young human subjects. As the clinical usefulness of selective alpha 1-adrenergic inhibitors is theoretically greater in states accompanied by increased sympathetic activity, the idea that selective alpha 1-adrenergic inhibition might be particularly useful in treating simultaneous hypertension and prostatism in older men has a sound physiological rationale.

Adrenergic alpha-Antagonists↗
PubMed1992

Effect of cold exposure and nutrient intake on sympathetic nervous system activity in rat kidney.

Renal sympathetic nervous system (SNS) responses to environmental temperature and diet were evaluated using [3H]norepinephrine ([3H]NE) turnover as the index of sympathetic activity. Pharmacological studies first demonstrated that renal NE was localized principally within storage granules of renal sympathetic nerves and regulated by central sympathetic outflow. Acute exposure to cold (4 degrees C), which increased cardiac SNS activity (P < 0.00005), had no effect on renal SNS. A 48-h fast suppressed renal [3H]NE turnover by 37% (P = 0.00024) and cardiac [3H]NE turnover by 48% (P = 0.00608). Dietary supplementation with sucrose did not affect [3H]NE turnover in kidney in either of two separate experiments, although it increased cardiac NE turnover in both. On the other hand, lard feeding significantly increased [3H]NE turnover in both kidney and heart, whereas dietary protein supplementation exerted no effect on either renal or cardiac [3H]NE turnover. These studies demonstrate a unique pattern of sympathetic regulation in kidney, one which is highly responsive to fasting and dietary fat, but not to cold exposure or dietary sucrose.

Animals↗
PubMedDate not supplied

The sympathetic nervous system in chronic heart failure.

The sympathetic nervous system plays a pivotal role in the natural history of chronic heart failure (CHF). There is early activation of cardiac adrenergic drive, which is followed by an increasing magnitude of generalized sympathetic activation, with worsening heart failure. The adverse consequences predominate over the short-term compensatory effects and are mediated through downregulation of beta-receptor function and harmful biological effects on the cardiomyocyte. beta-blockers exert a beneficial effect on the natural history of CHF by attenuating the negative biological effects, restoring homogeneity of contractile/relaxant mechanisms, and reducing the risk of myocardial ischemia and arrhythmias. After pioneering work conducted over 20 years ago, numerous studies have shown the beneficial effects of beta-blockade on left ventricular function, and survival, morbidity, and mortality rates in CHF. Large-scale trials are underway to determine the overall benefits of beta-blockade in heart failure.

Adrenergic beta-Antagonists↗
PubMed2003

Interactions between leptin and the human sympathetic nervous system.

Results from animal experimentation suggest a 2-way interaction between leptin and the sympathetic nervous system, with leptin causing sympathetic activation and conversely, with the sympathetic system exercising regulatory feedback inhibition over leptin release. We have now tested this hypothesis in humans. In the absence of results from leptin infusions, to test for sympathetic stimulation of leptin release, we sought a quantitative naturalistic linkage of sympathetic activity with leptin plasma concentration across a broad range of leptin values in men of widely differing adiposity. Renal norepinephrine spillover was correlated with plasma leptin (r=0.628, P<0.01), but other measures of sympathoadrenal function did not. To test for sympathetic and adrenomedullary inhibition of leptin release, we studied clinical models of high sympathetic tone, heart failure, and essential hypertension, in which lowered plasma leptin levels might have been expected but were not found; a model of low sympathetic activity, pure autonomic failure, in which plasma leptin level was normal (6.1+/-1.2 vs 12.8+/-3.1 ng/mL in healthy subjects); and a clinical model of reduced epinephrine secretion, healthy aging, in which plasma leptin level again was normal (5.7+/-1.1 ng/mL vs 4.0+/-0.9 ng/mL in men >60 years and <35 years, respectively). Paradoxically, leptin concentration was elevated in heart failure, caused entirely by reduced renal clearance of leptin release, 142.0+/-30.5 mL/min, compared with 56.9+/-18.9 mL/min (P<0.05). These results provide some support for the view that leptin stimulates the sympathetic nervous system, at least for renal sympathetic outflow, but do not confirm the concept of regulatory feedback inhibition of leptin release by the sympathetic nervous system.

Adult↗
PubMed1979

The effects of perhexiline on the sympathetic nervous system.

The effects of perhexiline on sympathetic nervous system function were studied in vitro and in vivo. Perhexiline decreased the field stimulation-induced contractile response of the isolated vas deferens and significantly decreased the quantity of norepinephrine released during stimulation of this preparation. In vivo studies in dogs showed that perhexiline reduced the heart rate response to cardiac accelerator nerve stimulation, an effect not associated with an increase in cholinergic tone or beta adrenergic blockade. Measurements of norepinephrine released from the heart during cardiac nerve stimulation showed that perhexiline (3 mg/kg) decreased norepinephrine release by approximately 35%. These results suggest that a presynatpic effect of perhexiline, which results in a decrease in norepinephrine release, contributes significantly to the attenuated heart rate response which occurs after administration of this drug. A decrease in transmitter release during sympathetic stimulation could play an important role in the mechanism for the protective effects of perhexiline in myocardial ischemic damage.

Animals↗
PubMed1995

Chronic hyperinsulinaemia and hypertension: the role of the sympathetic nervous system.

OBJECTIVE: To determine the implication of the sympathetic nervous system in the relationship observed between insulin resistance and hypertension. DESIGN: Rats were chronically treated with insulin for 12 days by subcutaneously implanted osmotic pumps and given 10% glucose in their drinking water. A separate group of rats also received glucose only, and control rats received tap water. RESULTS: Physiological hyperinsulinaemia (1.5 and 4.5 mU/kg per min insulin) increased mean arterial pressure by approximately 10 mmHg and heart rate by 60 beats/min, and supraphysiological insulinaemia (9 mU/kg per min) did not produce additional haemodynamic effects. Insulin-treated rats developed insulin resistance, as shown by an intravenous glucose-tolerance test. Glucose treatment alone induced intermediate haemodynamic and metabolic responses. Plasma noradrenaline levels rose slightly in insulin-treated rats and were positively correlated with mean arterial pressure but not with insulinaemia, even though insulinaemia was also correlated with mean arterial pressure. The reflex sympathetic activation during hypotension revealed, in the presence of a noradrenaline uptake antagonist, that insulin increases noradrenaline release but also enhances noradrenaline uptake. Chronic hyperinsulinaemia did not alter the sympathetic vascular and cardiac responses, as assessed by the measurement of the second messengers produced by activation of alpha 1- or beta-adrenergic receptor pathways. CONCLUSION: Chronic euglycaemic hyperinsulinaemia seems to modify sympathetic activity through several mechanisms, and this action could participate in the elevation of blood pressure observed in this rat model.

Animals↗
PubMed1986

Validation of a simple method of assessing cardiac preejection period: a potential index of sympathetic nervous system activity.

Traditional noninvasive assessment of sympathetic nervous system (SNS) activity in cardiovascular functioning has been confounded by concurrent parasympathetic influences. Analyses of specific intervals of the cardiac cycle have indicated that the systolic preejection period (PEP) may serve as a reliable index of SNS activity independent of parasympathetic inhibition. In the present study, PEP values derived from a technique employing peripheral pulse wave tracings were compared to values obtained from simultaneous impedance cardiograph recordings. Recordings were made on 15 male subjects who were instructed to rest quietly sitting in an upright position. Results indicated that values obtained from both methods were highly correlated and not significantly different when measurement adjustments on total systole were taken into account. These findings support the validity of the fingertip peripheral-pulse method in obtaining measures of systolic time intervals under resting conditions.

Adolescent↗
PubMed1994

Temporal changes in left ventricular function after massive sympathetic nervous system activation.

Intense activation of the sympathetic nervous system (SNS) decreases the contractile state of the rabbit left ventricle (LV). In this study, we determined the time course of LV dysfunction after massive central activation of the SNS in dogs. Veratrine (40-80 micrograms/kg) was injected intracisternally to activate the SNS in six chloralose-anesthetized dogs, and LV end-diastolic pressure (LVEDP), cardiac output, heart rate, and aortic pressure (Pa) were measured at 30-min intervals for 3 h. Pa increased from 147 +/- 8 (SE) to 272 +/- 7 mmHg (1 mmHg = 133.3 Pa) within 15 min, then declined to 148 +/- 16 mmHg by 1 h LV function curves (stroke work versus LVEDP or stroke work verus LV transmural pressure) showed a marked decrease in slope and a shift to the right within minutes after activating the SNS, which persisted for the duration of the experiment. These data indicate that LV contractility was diminished in these animals. No changes in LV function were observed in three dogs serving as time-matched controls. In three additional dogs, LV pressure was raised to a degree similar to that observed after SNS activation by constricting the ascending aorta for 1 h. These animals exhibited only modest shifts in the LV function curve during and after aortic constriction. Mean plasma catecholamine concentration increased by one to two orders of magnitude in animals after SNS activation, but only minor changes were observed in the other two groups. We conclude that myocardial contractility declines markedly soon after massive SNS activation and is not solely a function of the initial hypertensive period.

Acidosis↗
PubMed1990

Morphology of experimental tumors of the sympathetic nervous system.

The morphology of experimental tumors of the sympathetic nervous system in rabbits and hamsters induced by administration of nitrose compounds and the use of modifying factors were studied. The tumors were localized in the mediastinum, retroperitoneal space, adrenals and kidneys. A predominant involvement of the female animals was observed. Histological, histochemical and electron microscopic studies of 33 tumors of the sympathetic nervous system were carried out. By their degree of maturity the tumors were classified as ganglioneuromas, ganglioneuroblastomas and neuroblastomas. By their structure the experimental tumors were similar to the analogous neoplasias of man.

Animals↗