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At least 19 recordsLinked to original sources
PubMed1990

Interrelationships among the renin-angiotensin system, sympathetic nervous system and atrial natriuretic peptide in end-stage renal failure.

Since it remains unclear how the regulatory mechanism of blood pressure and volume is associated with the renin-angiotensin system, the sympathetic nervous system, and atrial natriuretic peptide (ANP), we examined the changes in blood pressure and vasoactive hormones occurring in 12 patients with end-stage renal failure. They were divided into two groups, those who were anuric (group A, n = 7), and those who had a daily urine volume of more than 700 ml (group B, n = 5). The changes in the mean blood pressure (MBP) and these vasoactive hormones were observed during hemodialysis with water removal in group A and without water removal in group B, and during blood pressure reduction with sodium nitroprusside in group A. The basal levels of ANP in groups A and B were twice as high as those of normotensive subjects. During hemodialysis, MBP did not reveal any changes in both groups. In group A, ANP and body weight (BW) decreased, whereas the plasma renin activity (PRA) and norepinephrine (NE) increased. In group B, ANP remained stable during the first 3 hr and decreased at the end of hemodialysis. However, BW, PRA, and NE were unchanged. In group A, significant correlations were observed between the changes in BW and those in ANP (r = 0.52, p less than 0.05), PRA (r = -0.57, p less than 0.01), and NE (r = -0.76, p less than 0.01). During blood pressure reduction, MBP decreased with accompanying increases in NE and PRA. However, ANP did not show any change.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1978

Nephrotoxic nephritis in rabbits. The role of the sympathetic nervous system.

The sympathetic nervous system and catecholamines play a major role in fibrin deposition in organs in rabbits after endotoxin administration. Glomerular fibrin deposition is also a key factor in the pathogenesis of nephrotoxic nephritis in rabbits, but the role of the sympathetic nervous system in this type of fibrin deposition has not been defined. We investigated sympathetic nervous system involvement in nephrotoxic nephritis using a model of isolated chemical sympathectomy with 6-hydroxydopamine. Different quantities of pooled nephrotoxic serum were injected intravenously into control and sympathectomized rabbits to produce a known spectrum of pathology in normal rabbits. Animals were killed and their organs were analyzed to ascertain that sympathectomy had been accomplished. Biochemical, immunohistologic, and histopathologic evaluation of the animals, comparing controls and sympathectomized rabbits, revealed no differences in the degree of renal damage for a given quantity of nephrotoxic serum. We conclude that, in the rabbit model, the sympathetic nervous system plays no significant role in the pathogenesis of fibrin deposition and glomerular damage in nephrotoxic nephritis.

Animals↗
PubMed1992

Persistence of a hyperdynamic circulation in cirrhotic rats following removal of the sympathetic nervous system.

The sympathetic nervous system is thought to play a role in the pathogenesis of the hyperdynamic circulation associated with portal hypertension. However, the extent of this role is unknown. After elimination of all neurological control by pithing, systemic and regional hemodynamics were studied in rats with portal hypertension caused by either portal vein stenosis or biliary cirrhosis. In normal rats, pithing induced a two-thirds decrease in mean arterial pressure and cardiac index. Compared with pithed normal rats, pithed portal vein-stenosed rats showed similar values for mean arterial pressure, cardiac index, and portal tributary blood flow. In contrast, pithed cirrhotic rats still showed hyperdynamic circulation with increased cardiac index and portal tributary blood flow. Although pithing dramatically reduced portal pressure in all groups, portal pressure remained significantly higher in portal hypertensive rats than in normal rats. These results indicate that in rats with portal vein stenosis, the sympathetic nervous system plays a major role in hemodynamic alterations, whereas in rats with cirrhosis, nonneurogenic factors participate in the pathogenesis of the hyperdynamic circulation.

Animals↗
PubMed1989

Metabolic factors and the sympathetic nervous system.

The sympathetic nervous system helps regulate both physiologic and metabolic functions. Norepinephrine usually mediates the physiologic functions, including heart rate, myocardial contractility, vasomotor tone, and blood pressure. Epinephrine produces the metabolic effects--including hyperglycemia, hyperlactacidemia, hyperlipemia, increased oxygen consumption, and serum potassium changes. Many of the metabolic effects are common to hypertension. Understanding the metabolic effects of the catecholamines could lead to understanding their role in disease states and thus to knowing the usefulness and risks of drugs that either mimic or block their action. The data presented were selected for their relevance to the metabolic abnormalities commonly encountered among hypertensive patients. The sympathetic nervous system's effects on glucose homeostasis, lipoprotein metabolism, potassium homeostasis, hyperinsulinemia, and hypertension are discussed.

Adrenal Glands↗
PubMed1989

Electrophysiology of ganglionic transmission in the sympathetic nervous system.

The sympathetic nervous system contributes to the regulation and control of a great number of body functions. A considerable fraction of preganglionic fibers are constantly discharging nerve impulses, and this tonic activity is responsible for a number of sustained bodily conditions. These tonic sympathetic discharges are of central origin and may be decreased by inhibition or augmented by excitation of the central neural mechanisms in control of the relevant preganglionic neurons. Certain other sympathetic paths become active only when special conditions lead to excitation of their central connections. The effect of the activity of preganglionic fibers on the different target organs, however, does not depend entirely on central regulatory influences. The sympathetic ganglia play a significant role processing and integrating the information arriving from the central nervous system and controlling the output to the target organs. In this context, the different potentials described above constitute the basis for the integrative process to occur. We now have substantial information about the basic biophysical events associated with different electrical events in the sympathetic ganglia. Very little is known, however, about how they operate in an integrative manner to control specific functions. The control of sympathetic responses during surgical stimulation is an important goal of general anesthesia. General anesthetics may operate to produce this effect at both central and peripheral levels. The sympathetic ganglion as a peripheral synapse, with basic integrative properties similar to the complex central nervous system, is a model still not sufficiently exploited to understand mechanisms by which general anesthetics control sympathetic response. The relevance of the findings described above in a variety of clinical situations, such as stress, hypertension, exercise, and anesthesia, remains to be studied.

Animals↗
PubMed1988

Modulation of functional capacity and survival in congestive heart failure. Effects of activation of the sympathetic nervous system.

Although the sympathetic nervous system is markedly activated in most patients with congestive heart failure, it is not clear whether such activity is clinically beneficial (and should be reinforced) or detrimental (and should be pharmacologically blocked). Some insights pertinent to this important question can be gained by reviewing the results of clinical trials with beta agonists and antagonists. Neither beta 1-selective (prenalterol) nor beta 2-selective (pirbuterol) agonists have been shown to be effective in treating heart failure in double-blind, placebo-controlled studies; moreover, research has indicated that prolonged stimulation of beta receptors with oral or intravenous catecholamines may adversely affect survival. In contrast, sustained therapy with drugs that attenuate the effects of the sympathetic nervous system (by blocking either tyrosine hydroxylase or beta-adrenergic receptors) may produce hemodynamic and clinical improvement and may favorably affect long-term prognosis. These potential benefits of beta-adrenergic blockade contrast strikingly with the lack of efficacy (with respect to clinical status and survival) of agents that block alpha-adrenergic receptors. Beta-adrenergic blockade carries important risks in the patient with heart failure, however. The risk-to-benefit ratio cannot be delineated accurately until the outcome of additional randomized clinical trials is known.

Adrenergic alpha-Antagonists↗
PubMed1990

The effects of captopril on the renin-angiotensin system and the sympathetic nervous system during sodium nitroprusside-induced hypotension in the halothane-anesthetized rabbit.

Three groups of New Zealand white rabbits were used to study the effects of captopril on the renin-angiotensin system and sympathetic nervous system during sodium nitroprusside (SNP)-induced hypotension and halothane anesthesia. Two groups of rabbits (C and CH) were treated with captopril 2 mg/kg i.v. One captopril-treated group (CH) and the third, untreated group (H) received SNP to induce hypotension. In these two groups, the mean arterial blood pressure (MAP) was reduced by 40% for 150 min. Group C did not undergo SNP-induced hypotension and served to document the effects of captopril alone during the 150-min study period. Arterial blood samples for norepinephrine (NE), epinephrine (EPI), and plasma renin activity (PRA) were drawn prior to, during hypotension, and in the recovery period. The SNP dose required to maintain the hypotension was continuously recorded. NE, EPI, and PRA all increased in group H, indicating activation of both the renin-angiotensin system and the sympathetic system during hypotension. This was accompanied by a dramatic increase in SNP dose requirement. In the CH group, PRA levels rose sharply and remained elevated. Plasma NE levels increased, while EPI levels remained unchanged with a decline in the SNP dose requirement. The C group demonstrated a rise in PRA levels, accompanied by unchanged NE and EPI levels and MAP during the study period. Captopril administration decreased the SNP dose requirement and significantly decreased the sympathetic response (measured by NE and EPI levels) in group CH as compared to the H group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1992

The influence of captopril on the epinephrine response to insulin-induced hypoglycemia in humans. The interaction between the renin-angiotensin system and the sympathetic nervous system.

The aim of this study was to assess whether an interaction exists between the renin-angiotensin system and the sympathetic nervous system at the level of the adrenal medulla during insulin-induced hypoglycemia in normal humans. Seventeen healthy volunteers were studied in a randomized, single-dose, double-blind, cross-over fashion using 25 mg captopril v placebo followed by an intravenous injection of 0.15 IU/kg insulin. Blood samples were obtained before and at 15 min intervals after insulin injection. Both plasma glucose level and heart rate were identical during captopril and placebo at rest and after insulin. Plasma renin activity increased after insulin and captopril. The increase in plasma epinephrine was lower after insulin and captopril compared to after insulin and placebo. Likewise the increase in plasma norepinephrine was blunted on insulin and captopril. Thus, when the generation of angiotensin II was blocked by captopril the insulin-induced rise in epinephrine and norepinephrine was blunted. This indicates that an interaction exists between the renin-angiotensin system and the sympathoadrenal system.

Adult↗
PubMed1986

Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system.

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Coronary arteriolar vasoconstriction in myocardial ischaemia: reflexes, sympathetic nervous system, catecholamines.

The sympathetic nervous system exerts important control over the coronary circulation. Studies from our laboratory have demonstrated that reflex input from skeletal muscle during static contraction causes coronary vasoconstriction. Similarly, stimulation of abdominal visceral chemosensitive afferents can, on occasions, elicit coronary vasoconstriction or limit the extent of vasodilation so that the myocardium needs to extract additional oxygen from arterial blood. Recently, we have examined the innervation of the coronary collateral circulation and found that these vessels contain catecholamines which demonstrate a pattern of fluorescence similar to that of catecholamines in the native circulation. Furthermore, stimulation of alpha 2- but not alpha 1-adrenoceptors can cause an increase in collateral vascular resistance. Thus, reflex input into the coronary circulation, perhaps during static exercise or post-prandially, can cause coronary vasoconstriction. Such constriction occurs in native coronary vessels and has the potential to be present in the coronary collateral circulation.

Animals↗
PubMed1988

Contribution of the renin-angiotensin system and of the sympathetic nervous system to blood pressure homeostasis during chronic restriction of sodium intake.

In a previous paper, we showed that during a long-term, moderate restriction in sodium intake, sympathetic nervous system activity was only transiently stimulated, whereas a sustained rise of plasma renin activity occurred. However, the contribution from stimulation of the renin-angiotensin system in the maintenance of blood pressure homeostasis during a low-salt diet is still unclear. To investigate this issue, in eight normal subjects blood pressure, heart rate, plasma catecholamines, renin activity, and aldosterone were measured during normal sodium intake (150 mEq/d), after converting-enzyme inhibition (enalapril 20 mg/d po), and during one month of sodium intake restriction (50 mEq/d) associated with chronic inhibition of converting-enzyme (CEI). During a low-salt diet with CEI, plasma renin activity rose significantly as a result of CEI. In addition, even in the presence of a marked and sustained increase in plasma norepinephrine and in upright heart rate, a decrease in blood pressure was observed in all the measurements performed during the course of the study as compared to the control values. Our findings support the hypothesis that renin-angiotensin system activation plays an important role in the maintenance of blood pressure homeostasis during a low-salt diet. In fact, in the presence of an effective blockade of angiotensin II formation, blood pressure is decreased, despite the concurrent, sustained stimulation of the sympathetic nervous system.

Adolescent↗
PubMedDate not supplied

Calcium channel blockade with nitrendipine. Effects on sodium homeostasis, the renin-angiotensin system, and the sympathetic nervous system in humans.

To test the hypothesis that the antihypertensive effect of the calcium channel blocking drug nitrendipine is in part related to natriuresis, we gave 16 subjects (8 normal, 8 hypertensive) placebo for 8 days followed by nitrendipine titrated to 20 mg twice daily for 8 days. The same diet was prepared for each meal for the entire study. Sodium intake was fixed for each subject and averaged 150 mEq/day. All urine was collected every day. Blood was drawn at the end of the placebo and nitrendipine periods for renin, aldosterone, and norepinephrine values. Nitrendipine caused a significant increase (p less than 0.05) in cumulative sodium excretion of 161 mEq over 7 days in the normal subjects and 103 mEq in hypertensive subjects. Potassium excretion was unaffected. In both hypertensive and normal subjects, plasma renin and plasma norepinephrine activity increased significantly (p less than 0.05), while plasma aldosterone levels did not change. Upright systolic blood pressure decreased significantly (p less than 0.05) in both groups, whereas upright diastolic blood pressure decreased only in hypertensive subjects. We conclude that blood pressure lowering effects of this drug may be in part related to natriuresis and that calcium channel blockade may dissociate plasma renin activity from that of aldosterone.

Adult↗
PubMed1989

Sympathetic nervous system activity and the heart.

The sympathetic nervous system has been viewed as the critical mechanism for cardiovascular response to increased circulatory needs during acute stress, augmenting cardiac rate and contractility and changing peripheral vascular tone. These physiologic responses, however, are increasingly thought to cause long-term adverse effects--such as altered myocardial function; renal, systemic, and coronary vasoconstriction; ventricular arrhythmias; and left ventricular hypertrophy--for some patients with cardiovascular disease. How the sympathetic nervous system affects the pathophysiology of cardiovascular diseases is not fully understood, although new techniques for assessing plasma catecholamines and for quantitating sympathetic activity are adding to our knowledge. Nevertheless, a review of the physiologic responses to sympathetic nervous system stimulation reveals much about their possible role in the cardiovascular disease process.

Animals↗
PubMed1992

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure.

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

Adrenal Medulla↗
PubMed1975

Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon. Influence of the sympathetic nervous system.

The influence of the sympathetic nervous system on the cerebral circulatory response to graded reductions in mean arterial blood pressure was studied in anesthetized baboons. Cerebral blood flow was measured by the 133Xe clearance method, and arterial blood pressure was decreased by controlled hemorrhage. In normal baboons, the constancy of cerebral blood flow was maintained until mean arterial blood pressure was approximately 65% of the base-line value; thereafter, cerebral blood flow decreased when arterial blood pressure was reduced. Superior cervical sympathectomy of 2-3 weeks duration did not affect the normal response. In contrast, both acute surgical sympathectomy (cervical trunk division) and alpha-receptor blockade (1.5 mg/kg of phenoxybenzamine) enhanced the maintenance of cerebral blood flow in the face of hemorrhagic hypotension in that cerebral blood flow did not decrease until mean arterial blood pressure was approximately 35% of the base-line value. The results indicate that the sympathetic nervous system is not involved in the maintenance of cerebral blood flow in the face of a fall in arterial blood pressure. Indeed, the implication is that the sympathicoadrenal discharge accompanying hemorrhagic hypotension is detrimental to, rather than responsible for, cerebral autoregulation.

Adrenergic alpha-Antagonists↗