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At least 19 recordsLinked to original sources
PubMed2003

Compared with control subjects, the systemic sympathetic nervous system is activated in patients with mitral regurgitation.

BACKGROUND: Whether the systemic sympathetic nervous system is activated as a compensatory mechanism in response to mitral regurgitation (MR) in humans is unknown. We tested the hypotheses that the systemic sympathetic nervous system would be activated in patients with MR in comparison with control subjects and that this activation would occur early in the disease process as a compensatory mechanism for chronic left ventricular (LV) volume overload. METHODS: We studied 37 patients with MR who underwent right heart catheterization and biplane cineventriculography to obtain LV end-diastolic and end-systolic volumes, ejection fractions, and regurgitant volumes. In these 37 patients with MR and in 23 control subjects, an [(3)H]-norepinephrine ([(3)H]-NE) infusion and multiple arterial blood samples provided data for a 2-compartment modeling analysis to calculate extravascular NE release rates (NE(2)). RESULTS: The mean NE(2) (2.05 +/- 0.76 microg/min/m(2)) in the patients with MR was greater than that in the control subjects (1.48 +/- 0.75 microg/min/m(2), P =.007). Furthermore, the mean NE(2) values were also greater in the patients with MR who were in clinical class I (P =.05), with a pulmonary capillary wedge pressure <12 mm Hg (P =.05) or a LV ejection fraction >or=0.60 (P =.06) compared with the control subjects. The mean NE(2) values were increased further in patients with MR who had a LV ejection fraction <0.60 (P =.02). CONCLUSIONS: The systemic sympathetic nervous system is activated in patients with MR in comparison with control subjects, and this activation appears to occur early in the disease process as a compensatory mechanism for LV volume overload.

Adult↗
PubMed2000

Relation of systemic sympathetic nervous system activation to echocardiographic left ventricular size and performance and its implications in patients with mitral regurgitation.

We have previously demonstrated that the systemic sympathetic nervous system (SNS) is activated in proportion to an increase in cineventriculographic left ventricular (LV) end-systolic volume and decrease in ejection fraction (EF) in patients with chronic mitral regurgitation (MR). However, the relation between noninvasive echocardiographic measures of LV size and performance and systemic SNS activation and their clinical implications in patients with MR is not known. We studied 17 MR patients with echocardiography, arterial norepinephrine (NE) sampling, and [3H]-NE infusions and arterial blood sampling to determine NE kinetic parameters using a 2-compartment analysis, including extravascular NE release rates (NE2, index of SNS activity) and the metabolic clearance rate from the vascular compartment. The arterial NE values correlated with LV end-systolic dimensions (r = 0.50, p = 0.04), but not with LV end-diastolic dimensions, and EF or fractional shortening measures. The NE2 values correlated with LV end-systolic dimensions (r = 0.53, p = 0.03) and inversely with LVEF (r = -0.45, p = 0.07) and fractional shortening (r = 0.43, p = 0.08) measures, but not with LV end-diastolic dimensions. The metabolic clearance rate values showed an inverse correlation with LV end-diastolic (r = -0.52, p = 0.03) and end-systolic (r = -0.49, p = 0.04) dimensions, but not with LV performance measures. The increase in NE2 values was progressive as the LV endsystolic dimensions increased and more marked at LV end-systolic dimensions > or = 40 mm. Thus, activation of the SNS is related to an increase in echocardiographic LV end-systolic dimensions and a decrease in LV performance measures in chronic MR. Medica, Inc.

Adult↗
PubMed2004

Changes in systemic sympathetic nervous system activity after mitral valve surgery and their relationship to changes in left ventricular size and systolic performance in patients with mitral regurgitation.

BACKGROUND: We have shown that the systemic sympathetic nervous system (SNS) is activated in patients with chronic mitral regurgitation (MR). However, the fate of systemic SNS activity after surgical correction of MR is currently unknown. METHODS: We examined 14 patients with MR who had normal sinus rhythm with an investigational, preoperative cardiac catheterization, including arterial norepinephrine (NE) sampling and [(3)H]-NE infusions and arterial blood sampling to determine NE kinetic parameters using a 2-compartment modeling analysis. The arterial NE and NE kinetic parameters were determined in all patients after mitral valve surgery (MVS) at a mean of 12 months. A 2-dimensional echocardiographic examination was also performed before and after MVS. RESULTS: The average extravascular NE release rates (NE(2)) before and after MVS were 1.89 +/- 0.66 and 2.26 +/- 0.82 microg/min/m(2) (P =.24), respectively. The average left ventricular (LV) end-diastolic dimension, fractional shortening, and ejection fraction decreased, whereas the mean LV end-systolic dimension did not change between the pre- and post-MVS echocardiographic studies. However, these group averages were comprised of patients with MR in whom the NE(2) and echocardiographic values both increased and decreased. This lack of homogeneity was a reflection of our new observation that the pre- to post-MVS changes in NE(2) were directly proportional to the changes in LV end-systolic dimension (r = 0.91, P <.001) and inversely related to the changes in LV fractional shortening (r = -0.82, P <.001) and ejection fraction (r = -0.78, P <.001). CONCLUSIONS: The response in systemic SNS activity in patients with MR after MVS is not homogeneous, and these changes are concordant with the post-MVS changes in LV size and systolic performance. These data further support our earlier observations and extend them to suggest that systemic SNS activation in patients with chronic MR is related to LV remodeling and impaired systolic performance.

Adult↗
PubMed1998

Opioid mediated effects on the immune system: sympathetic nervous system involvement.

Opioids have been hypothesized to suppress parameters of immune function by acting within the central nervous system to increase the activity of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Production of catecholamines and adrenocorticoids have been demonstrated to be responsible for many of the observed immunomodulatory effects which occur following opioid administration. In general, the sympathetic nervous system has been shown to play a role in regulating lymphocyte proliferation and natural killer cell activity as well as several other parameters of immune function. Here, we will focus primarily on the role of the sympathetic nervous system in modulating opioid induced immunosuppression. The role of the hypothalamic-pituitary adrenal axis is reviewed elsewhere in this issue.

Animals↗
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↗
PubMed1997

[Sympathy and heartache: new information on the sympathetic nervous system].

The sympathetic nervous system is an important regulator of the circulation. Interactions with other regulating systems, e.g. the renin angiotensin system, play important roles. By means of microneurography, sympathetic activity in humans can be assessed directly in the nerve. Insights into the dynamic regulation of the circulation under physiological and pathophysiological conditions are possible. Activation of the sympathetic nervous system in cardiovascular diseases affects course, prognosis, and therapy. Prognosis in heart failure depends on sympathetic activation, which can be decreased by inhibition of angiotensin II synthesis by ACE-inhibitors. In contrast to nitrates, these drugs do not increase sympathetic activity. The sympathetic nervous system is also heavily involved in the pathogenesis of hypertension. Borderline hypertensives and offspring of hypertensive parents show increased sympathetic nerve activities. Investigation of the sympathetic nervous system under physiological and pathophysiological conditions may serve as a basis for new therapeutic strategies.

Cardiovascular Agents↗
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↗
PubMed1993

Essential organization of the sympathetic nervous system.

The sympathetic nervous system consists of efferent neurones supplying the viscera. The cell bodies of preganglionic neurones are located in four areas in the thoracolumbar cord; however, the majority are found in the IML. Various tracing techniques have provided information concerning the location of the cell bodies of sympathetic preganglionic neurones projecting into various nerves and ganglia and regulating the adrenal gland, the kidney and the sympathetic supply to skeletal muscle. Numerous supraspinal neurones project to the neuropil surrounding sympathetic preganglionic neurones and may form synaptic contacts with these neurones. The areas of the brain that project to the IML appear to be part of a network of reciprocally connected supraspinal cell groups. Although much emphasis has been placed on the importance of the RVLM in the mediation of tonic and phasic inputs to sympathetic preganglionic neurones, it appears that other areas are of significant import; the RVLM should not be considered to be 'the vasomotor centre'. Spinal and cranial afferents influence the sympathetic nervous system. Baroreceptor afferents terminate in the NTS and may utilize an excitatory amino acid as their neurotransmitter. However, a number of neuropeptides are also associated with these afferents. Neurones within the NTS project to a number of brain stem areas thought to be involved in the regulation of sympathetic activity; consequently the baroreceptor reflex may be mediated over a number of parallel pathways involving both supraspinal and spinal sites of inhibition. Many neurotransmitters are thought to regulate the activity of sympathetic preganglionic neurons: monoamines, peptides and amino acids. Matching the chemical content of the cell bodies of neurones within a particular cell group with physiological characteristics is a challenging task; some barosensitive neurones of the RVLM do not appear to be adrenergic although they are in the midst of the C1 adrenergic cell group. Besides acetylcholine and noradrenaline, neurotransmission in the periphery appears to involve numerous peptides and ATP.

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↗
PubMed1999

Effects of antihypertensive therapies on the sympathetic nervous system.

The sympathetic nervous system is a major modulator of cardiovascular function. Over the past three decades, numerous studies, using various methodologies, have reported the existence of a variety of pre- and postsynaptic sympathetic dysfunctions in essential hypertension. Most of these abnormalities facilitate sympathetic neurotransmission, resulting in a chronic increase in the sympathetic tone and reactivity in a significant proportion of hypertensive patients. Chronic sympathetic activation is also associated with major alterations in the balance among postsynaptic adrenergic receptors in cardiovascular tissues. Indeed, an attenuation of beta-adrenergic function and a potentiation of alpha1-adrenergic function has been demonstrated in cardiovascular tissues in hypertensive patients, suggesting the development of a sympathetic postsynaptic alpha1 dominance during the development and evolution of hypertension. Chronic activation of the sympathetic system is deleterious and could contribute to the development of most cardiovascular complications associated with hypertension. One of the major aims of antihypertensive therapy should thus be to attenuate pre- or postsynaptic sympathetic tone. Most antihypertensive drugs have been found to improve either pre- or postsynaptic sympathetic function in hypertensive patients. At the presynaptic level, diuretics were found to increase the liberation of noradrenalin, presumably through baroreflex sympathetic activation. In contrast, beta-blockers were shown to attenuate noradrenalin release from sympathetic nerves by blocking presynaptic facilitatory beta-receptors, thus reducing the sympathetic tone on postsynaptic receptors. Similarly, angiotensin-converting enzyme inhibitors or angiotensin II type 1 (AT1) receptor antagonists have been found to reduce sympathetic reactivity by acting on the central nervous system, but also by blocking AT1-mediated facilitatory mechanisms located on sympathetic fibres and in the adrenal medulla. Short acting dihydropyridine calcium channel blockers (CCBs) were found to enhance noradrenalin release from sympathetic nerves, but longer acting CCBs seems to have variable effects. Indeed, while the chronic slow release formulation of nifedipine gastrointestinal therapeutic system (GITS) did not raise circulating noradrenalin levels, treatment with amlodipine increased circulating noradrenalin levels, suggesting that nifedipine GITS is neutral on the sympathetic tone but that amlodipine chronically activates the sympathetic system. At the postsynaptic level, however, dihydropyridine CCBs were shown to attenuate the sympathetic tone on alpha1-adrenoceptors. In conclusion, it appears that most antihypertensive drugs interfere with pre- or postsynaptic sympathetic mechanisms and that these mechanisms could contribute to their hypotensive effects.

Adrenergic Antagonists↗
PubMed2000

Antihypertensive drugs and the sympathetic nervous system.

The sympathetic nervous system (SNS) plays an important role in the regulation of blood pressure homeostasis and cardiac function. Furthermore, the increased SNS activity is a predictor of mortality in patients with hypertension, coronary artery disease and congestive heart failure. Experimental data and a few clinical trials suggest that there are important interactions between the main pressor systems, i.e. the SNS, the renin-angiotensin system and the vascular endothelium with the strongest vasoconstrictor, endothelin. The main methods for the assessment of SNS activity are described. Cardiovascular drugs of different classes interfere differently with the SNS and the other pressor systems. Pure vasodilators including nitrates, alpha-blockers and dihydropyridine (DHP)-calcium channel blockers increase SNS activity. Finally, central sympatholytics and possibly phenylalkylamine-type calcium channel blockers reduce SNS activity. The effects of angiotensin-II receptor antagonists on SNS activity in humans is not clear; experimental data are discussed in this review. There are important interactions between the pressor systems under experimental conditions. Recent studies in humans suggest that an activation of the SNS with pure vasodilators in parallel increases plasma endothelin. It can be assumed that, in cardiovascular diseases with already enhanced SNS activity, drugs which do not increase SNS activity or even lower it are preferable. Whether this reflects in lower mortality needs to be investigated in intervention trials.

Animals↗
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↗
PubMed1994

Vascular renin-angiotensin system and sympathetic nervous system activity in human hypertension.

Experimental data indicate the existence of a vascular tissue renin-angiotensin system in several different vessels from various animal models. Active renin can be locally synthesized into the vessel wall or taken up from circulating plasma to produce vascular angiotensin II. Using the human forearm technique, we produced evidence indicating the release of active and inactive renin and of angiotensin II from the vessels of hypertensive patients. Moreover, the production of vascular angiotensin II seems to be strictly correlated to the circulating renin profile, suggesting the possibility that vascular renin might be at least partially taken up from plasma. To investigate a possible function of the vascular renin-angiotensin system, we studied its interaction with sympathetic neurotransmission in essential hypertensive patients. In line with animal studies, vascular angiotensin II increases the vasoconstriction induced by the stimulation of the sympathetic nervous system through the potentiation of noradrenaline release at a presynaptic level, and this effect seems to be mediated by beta-adrenoceptor activation. This facilitating effect on sympathetic neurotransmission exerted by vascular angiotensin II can be antagonized by both angiotensin II antagonists and angiotensin-converting enzyme inhibitors.

Blood Vessels↗
PubMed1986

Dissociation of the responses of the renin-angiotensin system and sympathetic nervous system to a vasodilator stimulus in congestive heart failure.

The ability of neurohumoral reflex control mechanisms to respond to a vasodilator mediated alteration in hemodynamic status was studied. A sodium nitroprusside infusion was administered to 5 normal subjects and 47 patients with severe congestive heart failure resulting in significant decreases in mean arterial pressure and in systemic vascular resistance. As expected in normals the vasodilator stimulus caused a reflex activation in both the renin-angiotensin system and sympathetic nervous system as measured by increased plasma renin activity and plasma norepinephrine, respectively. In the patients with heart failure, plasma renin activity rose similarly in response to nitroprusside (+63% in heart failure, 100% in normals, P = NS) while plasma norepinephrine remained essentially unchanged (+11% in heart failure, 98% in normals, P less than 0.01). These data demonstrate that the neurohumoral dysfunction seen in patients with heart failure is not uniform. In patients with severe congestive heart failure the renin-angiotensin system apparently is activated by mechanisms other than sympathetic nervous stimulation. This intact reflex humoral response may still function in opposition to the beneficial hemodynamic effects produced by direct vasodilators such as nitroprusside.

Adult↗
PubMed1980

Acute renovascular hypertension in conscious dogs. Interaction of the renin-angiotensin system and sympathetic nervous system in systemic hemodynamics and regional blood flow responses.

The effects of acute renovascular hypertension on the sympathetic nervous system, regional blood flow and cardiac function were studied in conscious dogs submitted to renal artery occlusion by inflation of a cuff implanted previously around one renal artery. We then compared the alterations in plasma renin and catecholamine levels and in the various hemodynamic parameters induced by those maneuvers in intact dogs, to those in dogs pretreated with alpha- and beta-adrenergic receptor blockers. Subsequently, the converting enzyme inhibitor teprotide was administered to inhibit angiotensin formation in both experiments. Our results suggest that both the renin-angiotensin system and the sympathetic system contribute to the rise in blood pressure. The hemodynamic changes and alterations in regional blood flows accompanying this acute hypertension appear to be due mostly to the increase in plasma angiotensin, since prior adrenoceptor blockade only attenuated their magnitude but did not alter their direction. However, angiotensin-induced coronary vasoconstriction was observed only in adrenergically blocked but not intact animals, probably because of the protective effect of baroreceptor-mediated reflex sympathetic coronary vasodilation.

Acute Disease↗