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At least 163 records · Page 9Linked to original sources
PubMed1993

Central and peripheral vasopressin interact differently with sympathetic nervous system and renin-angiotensin system in renal hypertensive rabbits.

This study was designed to elucidate how central and peripheral arginine vasopressin (AVP) interacts with the sympathetic nervous system and the renin-angiotensin system to maintain blood pressure in two-kidney, one-clip hypertensive rabbits. We recorded renal sympathetic nerve activity (RSNA) in the conscious state as an index of sympathetic nervous system function. The changes in mean arterial pressure, heart rate, and RSNA were recorded continuously for 60 minutes after intravenous administrations of captopril (2.5 mg/kg) and nicardipine (3.2 micrograms.kg-1.min-1) in eight identical rabbits. Despite equivalent reductions in mean arterial pressure (10 +/- 1 mm Hg), the increase in RSNA was significantly larger with captopril than that with nicardipine, and the plasma concentration of AVP was elevated (from 100% to 255 +/- 24%) with captopril. Mean arterial pressure was reduced, and RSNA was increased by intravenous infusion of AVP antagonist d(CH2)5Tyr(Me)AVP (n = 8), whereas vertebral artery infusion of the antagonist (n = 6) did not change RSNA. During central and peripheral infusions of AVP antagonist, RSNA was exaggerated by blood pressure reduction with nicardipine as well as with captopril. Increases in RSNA induced by captopril and nicardipine were larger by central infusion of AVP antagonist than by intravenous infusion. The decrease in mean arterial pressure by captopril (30 +/- 4 mm Hg) in eight sinoaortic-denervated hypertensive rabbits was larger than that in hypertensive rabbits with intact baroreflex. These data suggest that compensatory activation of RSNA was revealed by central and peripheral attenuation of AVP and that the sympathetic nervous system became the most important mechanism for blood pressure maintenance in the absence of AVP. The interaction of AVP with the sympathetic nervous system may be independent of the state of the renin-angiotensin system, since the exaggeration of RSNA by AVP antagonist was qualitatively the same with nicardipine as with captopril. In conscious renal-hypertensive rabbits, AVP in the central nervous system played a substantial role when blood pressure was reduced, although it did not contribute to blood pressure maintenance in the basal condition.

Angiotensin II↗
PubMed1989

Impaired sympathetic nervous system response to cognitive effort in early Alzheimer's disease.

Sympathetic nervous system responses to a cognitive challenge and a physiologic stimulus (upright posture) were compared in 10 patients with early Alzheimer's Disease and a group of healthy older adults. Plasma catecholamine and cardiovascular responses to upright posture were similar in the two groups. However, sympathetic activation during mental effort was impaired in the patient group; this difference did not appear to be attributable to motivational factors. Alzheimer's Disease is associated with a defect in sympathetic nervous system function that is specifically linked to cognitive effort and appears early in the course of the disease.

Aged↗
PubMed2002

Alterations of the sympathetic nervous system and metabolic performance of the cardiomyopathic heart.

Little is known about the effects of altered sympathetic innervation on the efficiency of the cardiomyopathic heart. Thus, it was the aim of this study to determine non-invasively the relationship between the metabolic cost of cardiac work and alterations of the sympathetic nervous system. In ten patients with chronic idiopathic dilated cardiomyopathy, left ventricular function and geometry were assessed by tomographic radionuclide angiography. Myocardial oxidative metabolism was quantified by the clearance constant k(mono) for carbon-11 acetate, determined by positron emission tomography (PET). Cardiac efficiency was then estimated by the work-metabolic index [WMI = stroke volume index x heart rate x systolic pressure/k(mono)]. Additionally, myocardial presynaptic sympathetic innervation was investigated in the same PET session using 11C-hydroxyephedrine, and plasma norepinephrine levels were determined by high-performance liquid chromatography. The WMI was 3.0+/-1.3 mmHg x ml x 10(6)/m2 and correlated significantly with left ventricular ejection fraction (19%+/-10%; r=0.66, P<0.04) and peripheral vascular resistance (3,638+/-1,085 dynes x s/cm5; r=-0.75, P<0.01). Cardiac hydroxyephedrine retention, reflecting integrity of presynaptic innervation, was abnormally low in 58%+/-38% of the left ventricle. Cardiac hydroxyephedrine retention (r=0.65, P<0.05) and plasma norepinephrine concentration (r=-0.80, P<0.01) both correlated significantly with the WMI. At multivariate stepwise linear regression, only plasma norepinephrine and peripheral vascular resistance were independent determinants of the WMI. In conclusion, metabolic performance of the cardiomyopathic heart decreases with increasing alterations of the sympathetic nervous system. Increasing afterload and effects of systemic sympathetic activation, however, seem to play a dominant role while direct alterations of cardiac presynaptic sympathetic innervation are not independently associated.

Acetic Acid↗
PubMed1992

Role of the sympathetic nervous system in the alcohol-guanabenz hemodynamic interaction.

The present study evaluated the contribution of the sympathetic nervous system to the adverse hemodynamic action of ethanol on hypotensive responses in conscious unrestrained spontaneously hypertensive rats. Ethanol caused a dose-related attenuation of the hypotensive effect of guanabenz. An equivalent hypotensive response to sodium nitroprusside was not influenced by ethanol, which indicates a potential specific interaction between ethanol and guanabenz. Alternatively, it is possible that a preexisting high sympathetic nervous system activity, which occurred during nitroprusside infusion, may mask a sympathoexcitatory action of ethanol. Further, ethanol (1 g/kg) failed to reverse the hypotensive effect of the ganglionic blocker hexamethonium. This suggests that a centrally mediated sympathoexcitatory action of ethanol is involved, at least partly, in the reversal of hypotension. In addition, the antagonistic interaction between ethanol and guanabenz seems to take place within the central nervous system and involves opposite effects on central sympathetic tone. Finally, changes in plasma catecholamines provide supportive evidence for the involvement of the sympathetic nervous system in this interaction. In a separate group of conscious spontaneously hypertensive rats, ethanol (1 g/kg) reversed the guanabenz-evoked decreases in blood pressure and plasma catecholamine levels. It is concluded that (i) ethanol adversely interacts with centrally acting antihypertensive drugs through a mechanism that involves a directionally opposite effect on sympathetic activity, and (ii) a sympathetically mediated pressor effect of ethanol is enhanced in the presence of an inhibited central sympathetic tone.

Animals↗
PubMed1989

The relationship of the sympathetic nervous system and the renin-angiotensin system in congestive heart failure.

Congestive heart failure is a complex clinical syndrome characterized by circulatory and metabolic abnormalities. It has been apparent for more than 25 years that the sympathetic nervous system and the renin-angiotensin-aldosterone system are markedly activated in the late stages of heart failure. These two systems interact to facilitate sympathetic drive and promote salt and water retention. Circumstantial evidence is now accumulating to indicate that excessive sympathetic drive and angiotensin II activity may contribute to the pathophysiology of heart failure. These observations suggest that a dual strategy of modulating sympathetic nervous system activity to the heart while blocking angiotensin II activity may provide a rational therapeutic approach to the treatment of heart failure. Xamoterol, a beta 1 partial agonist, may enhance myocardial contractile force in the steady state, while acting to inhibit excessive sympathetic drive during exercise or severe heart failure. The concomitant use of a converting-enzyme inhibitor would be expected to blunt the detrimental effects of excessive angiotensin II activity. Modulation of adrenergic drive coupled with inhibition of marked angiotensin II activity may be potentially more effective in the treatment of congestive heart failure than either strategy used alone.

Adrenergic beta-Agonists↗
PubMed1984

Effects of chronic beta-receptor stimulation on sympathetic nervous system activity, energy expenditure, and thyroid hormones.

The effects of hyper- and hypothyroidism on sympathetic nervous system activity and energy expenditure are well recognized. The impact of altered sympathetic nervous system activity on energy expenditure and thyroid hormone metabolism has not been well studied. We investigated the effects of orally administered terbutaline sulfate, a beta 2-receptor agonist (5 mg, three times per day for 2 weeks), on the activity of the sympathetic nervous system, energy expenditure, and thyroid hormone metabolism in six normal men, aged 21-36 yr. The cardiovascular, metabolic, and thermogenic responses to an infusion of the beta-adrenergic agonist isoproterenol were clearly blunted after 2 weeks of treatment with terbutaline sulfate, indicating down-regulation of beta-receptors and/or development of reduced sensitivity. There were no significant changes in the cardiovascular, metabolic, or thermogenic responses to an infusion of the alpha-adrenergic agonist phenylephrine. Basal metabolic rate was significantly increased by the chronic administration of terbutaline sulfate [5.040 +/- 0.167 (+/- SE) vs. 5.421 +/- 0.234 kJ/min; P less than 0.05]. There was a highly significant change in the serum T3 to T4 ratio (19.4 +/- 1.0 vs. 24.4 +/- 1.0; P less than 0.001). This was a result of increased serum T3 concentrations (136 +/- 9 vs. 160 +/- 14 ng/dl; P less than 0.05) and decreased serum T4 concentrations (7.2 +/- 0.8 vs. 6.7 +/- 0.8 micrograms/dl; P = NS). Chronic beta-receptor stimulation with terbutaline sulfate increases the basal metabolic rate and T3 concentrations. These changes occurred despite down-regulation of beta-receptors and/or decreased sensitivity in response to chronic terbutaline administration.

Adrenergic alpha-Agonists↗
PubMed2000

Sympathetic nervous system activity and cardiovascular homeostatis during head-up tilt in patients with spinal cord injuries.

The relationship between sympathetic nervous system activity and cardiovascular responses to head-up tilt in patients with spinal cord injuries and in able-bodied subjects was studied. Twenty-seven adults, nine in each of the three groups (tetraplegia, paraplegia, and able-bodied subjects) were tilted 70 degrees, head up, for 12 minutes after 20 minutes supine rest. Differences between steady-state measurements of mean arterial pressure, stroke volume, and sympathetic nervous system activity were estimated in both positions. Sympathetic nervous system activity was reflected by the low-frequency peak of the blood pressure variability spectrum. From supine rest to head-up tilt, low-frequency power increased in able-bodied subjects (median, 0.42 mm Hg2, p = 0.003), which was different (p = 0.015) from patients with tetraplegia and paraplegia (-0.15 and -0.10 mm Hg2, respectively). Stroke volume and mean arterial pressure decreased in patients with tetraplegia (-40% and -9 mm Hg, respectively; p = 0.008, both variables) more than in able-bodied subjects (-33%, 11 mm Hg, respectively) or patients with paraplegia (-24%, 8 mm Hg, respectively). Results indicated increased sympathetic nervous system activity during head-up tilt in able-bodied subjects, but not in patients with paraplegia or tetraplegia, whereas patients with tetraplegia, but not paraplegia, showed poorer cardiovascular homeostasis than able-bodied subjects. This suggests that patients with paraplegia maintained cardiovascular homeostasis during head-up tilt without increased sympathetic nervous system activity.

Adult↗
PubMed2002

The influence of aging on the human sympathetic nervous system and brain norepinephrine turnover.

Investigating aging effects on the sympathetic nervous system and ascertaining underlying central nervous system (CNS) mechanisms mediating sympathetic stimulation is clinically pertinent because of the possible interconnection of cardiovascular disease development with age-dependent sympathetic nervous changes. Because of previous evidence linking human CNS neuronal noradrenergic function and sympathetic activity, we investigated the influence of aging on brain norepinephrine turnover in 22 healthy men aged 20-30 yr and 16 healthy men aged 60-75 yr by measuring the internal jugular venous overflow of norepinephrine and its lipophilic metabolites. Sympathoneural and adrenal medullary function was also studied, using plasma catecholamine isotope dilution methodology and regional central venous sampling. In the older men there was increased norepinephrine turnover in suprabulbar subcortical brain regions, 317 +/- 50 ng/min compared with 107 +/- 18 ng/min in younger men. A differentiated sympathetic nervous activation was also present in older men. Overall, levels of both cardiac and hepatomesenteric norepinephrine spillover were directly correlated with subcortical norepinephrine turnover. These findings suggest that in sympathetic nervous activation accompanying aging, as has previously been demonstrated with the sympathetic nervous stimulation in human hypertension and heart failure, there is an underlying sympathoexcitatory influence of noradrenergic projections to suprabulbar subcortical regions.

Adult↗
PubMed2005

Increased intracranial pressure induces a rapid systemic interleukin-10 release through activation of the sympathetic nervous system.

There is a bi-directional communication between the immune and central nervous system. In this context, it is known that patients with traumatic brain injury suffered from systemic immunodepression and an increased risk to develop infectious complications. We investigated the role of an increased intracranial pressure (ICP) and sympathetic activation on systemic immune changes. A sustained increase in ICP was achieved by inflation of a subdural balloon. At different time points, plasma levels of the anti-inflammatory cytokine, interleukin (IL)-10, were measured. Furthermore, the effect of a sympathetic blockade by co-administration of the beta2-adreoreceptor antagonist, propranolol, was evaluated. Finally, we examined the impact of epinephrine infusion on blood IL-10 levels. We showed that an increase in ICP with activation of the sympathetic nervous system was able to induce systemic release of IL-10. This effect was blocked by administration of the beta2-adreoreceptor antagonist. Furthermore, epinephrine infusion directly induced systemic release of IL-10. Our data suggested that sympathetic activation with release of epinephrine may induce systemic immunodepression with risk of infectious complications in brain-injured patients.

Animals↗
PubMed1984

[Significance of the sympathetic nervous system for the coronary circulation].

The activation of sympathetic nerves plays a significant role in the initiation of acute myocardial ischemia. In this review the effects of sympathetic nerves on coronary blood flow are summarized. Under physiological conditions the increase in myocardial performance during sympathetic activation is accompanied by metabolic coronary vasodilation. The resulting increase in coronary blood flow is limited by about 30% by alpha-adrenergic coronary constriction. Extravascular compression and beta-adrenergic coronary dilation are of minor importance during sympathetic activation. With exhausted coronary reserve distal to severe coronary stenoses metabolic vasodilation during sympathetic activation is not possible any more; an alpha 2-adrenoceptor-mediated coronary vasoconstriction now predominates. This coronary constriction induces ischemia of the post-stenotic myocardium. The alpha-antagonists Phentolamine and Rauwolscine as well as the calcium-antagonist Nifedipine prevent poststenotic coronary constriction and myocardial ischemia. Also in the genesis of coronary arterial spasm the sympathetic nervous system may play an important role; the constriction of epicardial coronary arteries is mediated by alpha 1-adrenoceptors. The sympathetic nervous system is not only involved in the initiation of myocardial ischemia, but is also activated by ischemia. This feedback-activation of sympathetic nerves leads to an aggravation of myocardial ischemia.

Coronary Circulation↗
PubMed1984

The sympathetic nervous system in hypertension.

Sympathetic drive can contribute not only to the acute adjustment to circulatory stresses but also to sustained elevation in vascular resistance and arterial pressure. In hypertensive animals and humans excessive sympathetic activity coupled with a possible genetic factor may result in defects in electrogenic ion transport of vascular muscle or in excessive vascular hypertrophy. Increased sympathetic activity and release of the neurotransmitter may occur as a result of defects of the efferent, afferent or central components of the sympathetic system. Several studies in various animal models and in humans are described to support the notion that the mosaic concept in hypertension may be embodied in a dual theory that includes a vascular muscle defect coupled with excessive sympathetic drive both of which may be of genetic or acquired origin. Almost regardless of the cause of hypertension, interruption of sympathetic efferent activity lowers arterial pressure.

Afferent Pathways↗
PubMed2005

Sleep apnea in heart failure: implications of sympathetic nervous system activation for disease progression and treatment.

Mortality risk in heart failure relates to the degree of chronic sympathetic nervous system activation. Do acute increases in central sympathetic outflow, as occur nightly in patients with sleep apnea, augment this risk? This review explores 4 novel concepts: 1) sleep disordered breathing is common in heart failure, 2) the acute effects of sleep apnea and the chronic effects of heart failure on the sympathetic nervous system are additive when these conditions coexist, 3) such convergence has adverse clinical and prognostic implications, and 4) treating sleep apnea can attenuate sympathetic nervous system activation and improve ventricular systolic function.

Continuous Positive Airway Pressure↗
PubMed1991

Response of sympathetic nervous system activity to exercise in patients with congestive heart failure.

To investigate the serial sympathetic nervous system response to exercise, plasma norepinephrine (NE) and epinephrine (E) concentrations were measured at rest, during each stage of treadmill exercise, and immediately and 5 minutes after exercise in 68 congestive heart failure (CHF) patients (NYHA functional class I 24, II 25, III 19) and 30 normal subjects. Circulatory responses of NYHA class II patients increased at early stages of exercise. Systolic blood pressure and double product at peak exercise were significantly lower in NYHA class III patients. Plasma NE response of NYHA class I patients was similar to that of normal subjects. However, plasma NE at rest, and during and after exercise were significantly higher in NYHA classes II and III patients than in normal subjects and NYHA class I patients (peak NE (pg ml-1); Normals: 547 +/- 37, I: 535 +/- 53, II: 867 +/- 87, III: 1033 +/- 157). There was no significant difference in plasma E levels among the four groups. NE response to exercise was augmented according to the severity of heart failure, which suggested compensatory activation of sympathetic nervous system activity. Circulatory responses were reduced in NYHA class III patients despite the exaggerated compensatory activation of the sympathetic nervous system. Blunted circulatory responses to increased NE concentration in NYHA class III patients might relate to a decreased cardiac responsiveness to sympathetic activity in severe CHF patients.

Adult↗