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PubMed2004

Interactions between the sympathetic nervous system and the cardiac natriuretic peptide system.

The sympathetic nervous system (SNS) and the cardiac natriuretic peptide system (NPS) are fundamentally important neurohumoral systems for cardiovascular regulation. Their mutual interactions have been subject to numerous experimental and human studies. In the current manuscript, results from in vivo and in vitro studies will be reviewed with a focus on sympathetic outflow on the control of natriuretic peptide release.

Adrenergic beta-Antagonists↗
PubMed1993

[Age-related changes in the renin-angiotensin-aldosterone system and the sympathetic nervous system in patients with essential hypertension].

The aim of this study was to evaluate age, plasmatic renin activity (PRA), plasma aldosterone levels and the total quantity of urinary catecholamines (TOT. UR. CAT.) in a large population of out-patients suffering from essential arterial hypertension (EAH). A total of 986 patients were examined (540 women and 426 men aged between 15 and 87 years) suffering form slight or moderate EAH (WHO stage 1-2). After a wash-out period of two weeks, systolic and diastolic arterial pressure was measured together with heart rate in clino- and orthostatism. Blood samples were collected to determine PRA and plasma aldosterone, and lastly a 24-hour urine collection was made to measure the total quantity of catecholamines. It emerged that there was a significant increase in systolic pressure, whereas heart rate and PRA diminished significantly when correlated with age; diastolic pressure was also considerably lower, but did not reach statistical significance. Moreover, it was found that there was a significant positive correlation between PRA and TOT. UR. CAT., whereas no correlation was found between age and plasma aldosterone and between blood pressure and the various endocrine parameters examined. These data confirm the changes in the biological, hemodynamic and endocrine profiles observed in elderly hypertensive patients in comparison to young hypertensive patients, and suggests that age may be an important predictive factor of the activity of both the renin-angiotensin and sympathetic nervous system which appear to be closely connected and gradually attenuated by age.

Adolescent↗
PubMed2007

The sympathetic nervous system of anamniotes.

The sympathetic nervous system develops as an evolutionary trait with gnathostomes (jawed vertebrates), but not with agnathan fishes (i.e., hagfishes and lampreys). Organization of the sympathetic preganglionic neuronal columns is different in teleosts and anurans. In the teleosts so far examined, the majority of sympathetic preganglionic neurons (SPNs) are located in the dorsal part of the spinal central gray matter. In Tetraodontiformes, the cell column occupies only two rostral spinal segments, which are distinct in their cytoarchitecture and projections. On the other hand, the SPNs of anurans form two cell columns segregated mediolaterally. The lateral and medial columns are also distinct in their cytoarchitecture and projections. The neuroactive substances expressed in the SPNs both in teleosts and anurans are coded to the projections. In anurans, the SPNs containing gonadotrophin-releasing hormone and those containing calcitonin gene-related peptide are involved in the regulation of blood vessels and cutaneous glands, respectively. In the filefish, the SPNs containing galanin project specifically to non-adrenergic non-cholinergic postganglionic neurons in the cranial sympathetic ganglia. Therefore, both anuran and teleost systems have different morphological and chemical-coded patterns for functional variation, although the anuran sympathetic nervous system has more organizational similarity with that of amniotes.

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↗
PubMed1985

Influence of the parasympathetic and sympathetic nervous system on nocturnal bronchial obstruction.

To determine whether an autonomic nervous system imbalance might underlie the nocturnal dyspnoea in patients with chronic airflow obstruction (CAO), we determined FEV1, sinus arrhythmia gap (SA gap), heart rate and urinary adrenaline and noradrenaline excretion every 4 h over 24 h. Measurements were performed in eight non-allergic patients with CAO and eight age- and sex-matched normal controls. The amplitude of the circadian changes in FEV1 in patients and controls was 27 +/- 2% and 7 +/- 1% respectively (P less than 0.001). Both an increased SA gap and a decreased heart rate are features of increased vagal activity. This vagal activity was significantly increased in patients, compared with normal controls (difference P less than 0.01), the difference being maximal at night. This increased activity might contribute to a bronchial obstruction in these patients. Urinary adrenaline excretion was significantly higher by day than by night in both patients and normal controls (P less than 0.01). The urinary levels of adrenaline in the patients were significantly decreased at all hours of observation as compared with levels in normal controls (P less than 0.05). Urinary noradrenaline levels were significantly lower in patients as compared with normal subjects (P less than 0.01), and lower by night than by day. Urinary histamine and Nt-methylhistamine excretion were in the normal range in each individual. Urinary levels, however, were significantly higher in patients at all hours of observation (P less than 0.05). No circadian rhythm was shown. Plasma cortisol levels showed a normal circadian variation, similar in patients and normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Role of the parasympathetic nervous system and interaction with the sympathetic nervous system in the early phase of hypertension.

The role of the peripheral parasympathetic nervous system in the development of hypertension was investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Animals were 5-7 weeks old, anesthetized, and in the open-chest condition. The decrement in heart rate evoked by parasympathetic nerve stimulation (62 +/- 8 beats/min) in SHR was greater (p < 0.01) than that in WKY rats (23 +/- 4 beats/min). Furthermore, the decrease in heart rate (73 +/- 9 beats/min) in response to combined stimulation of sympathetic and parasympathetic nerves in SHR was greater (p < 0.05) than that in response to vagal stimulation alone. The extent of the interaction of sympathetic and parasympathetic nerves was calculated as the difference between the decrease in heart rate during combined stimulation and that during vagal nerve stimulation alone. The extent of the interaction in SHR (-11 +/- 5) was not significantly different from that in WKY rats (-8 +/- 3 beats/min). Therefore, the influence of the peripheral parasympathetic nervous system in the early phase of hypertension may be greater than that in the normotensive state. Interaction between the two branches of the autonomic nervous system may occur as accentuated antagonism originating in the early phase of hypertension. The interaction during the early phase of hypertension may not be different in extent from that of the normotensive state.

Animals↗
PubMed1984

[The effect of alterations of the renin-angiotensin system and the sympathetic nervous system on plasma bradykinin concentration in patients with essential hypertension].

We studied the possible interplay between plasma bradykinin (P-BK) and the renin-angiotensin axis in essential hypertension, the effect of catecholamine on P-BK by standing and norepinephrine (NE) infusion, and the possible role of bradykinin in the hypotensive mechanism of angiotensin I converting enzyme inhibitor (captopril) in renin-independent essential hypertension. Plasma bradykinin was measured by sensitive radioimmunoassay in 44 hypertensive patients and compared with that of 24 normotensive subjects. P-BK was not significantly reduced in hypertensive patients, and when subjects were divided by age range, the P-BK was reduced by aging in normotensive subjects but not in hypertensive patients, and the elder (60 approximately 80 yr) age normotensive group showed significantly (p less than 0.05) lower P-BK compared with the elder hypertensive group. 28 essential hypertensive patients (EHT) who were classified as WHO stageI (n=15) and WHO stageII (n=13) were given 80 mg of furosemide orally and kept upright for 4 hours. Plasma renin activity (PRA), P-BK, plasma aldosterone (P-Ald) and serum angiotensin converting enzyme activity (ACEA) were measured before and after furosemide administration. Twelve normotensive subjects served as controls. PRA, P-Ald and ACEA showed a significant increase (p less than 0.05) in all groups in response to furosemide. In normotensives, basal P-BK was 11.1 +/- 1.3 pg/ml which increased to 15.6 +/- 1.8 pg/ml (p less than 0.02) after furosemide. These changes of P-BK were in parallel with PRA, P-Ald and ACEA. In the WHO stageI EHT group, baseline P-BK was 9.7 +/- 1.3 pg/ml which increased to 15.6 +/- 1.8 pg/ml (p less than 0.02) and PRA, P-Ald and ACEA showed a similar increase as in normotensives. In the WHO stageII EHT patients, however, P-BK showed only a slight increase from 9.8 +/- 1.0 pg/ml to 12.0 +/- 1.1 pg/ml after furosemide. These changes were smaller either than normotensives or the WHO stageI EHT group. There was a slight but significant correlation between PRA and P-BK in normotensives and in the WHO stageI EHT. There was no correlation between PRA and P-BK in the WHO stageII EHT. The present results do not support the view that there may be a direct linkage between the kallikrein kinin system and the renin angiotensin axis mediated by kininase II or angiotensin converting enzyme in human peripheral blood.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1999

The effects of ramipril on sympathetic nervous system function in older patients with hypertension.

BACKGROUND: There are important interactions between the renin-angiotensin system and the sympathetic nervous system. Therapy with angiotensin-converting enzyme (ACE) inhibitors may suppress sympathetic nervous system activity. OBJECTIVE: To test the hypothesis that long-term ACE inhibition by ramipril will suppress sympathetic nervous system activity and up-regulate alpha-adrenergic receptor responsiveness in older patients with hypertension. METHODS: This placebo-controlled, double-blind randomized study was conducted at the University Hospital, General Clinical Research Center, University of Michigan Medical Center. Fifteen healthy older patients with mild to moderate hypertension received 8 weeks of ramipril therapy with doses ranging from 5 mg to 20 mg. The following measurements were obtained: plasma norepinephrine levels; norepinephrine kinetic parameters derived from plasma norepinephrine and 3H-norepinephrine levels obtained during infusion and disappearance of 3H-norepinephrine, including the extravascular norepinephrine release rate, norepinephrine clearance, spillover fraction, and volume of distribution; forearm blood flow; platelet membrane alpha2-receptor binding characteristics, and adenylyl cyclase activity. RESULTS: Although plasma norepinephrine levels increased in the subjects treated with ramipril, there were no significant differences from baseline in the rate of norepinephrine appearance into the vascular compartment (P = .76) or in the rate of norepinephrine release into the extravascular compartment (P = .92). In addition, no differences were observed in other norepinephrine kinetic parameters (norepinephrine spillover fraction, norepinephrine volume of distribution, or clearance) between the ramipril and placebo groups. Consistent with this, there was no apparent change in measures of vascular or platelet alpha-adrenergic receptor responsiveness. CONCLUSIONS: Ramipril therapy did not suppress systemic sympathetic nervous system activity, alter other norepinephrine kinetic parameters, or alter alpha-adrenergic responsiveness in older patients with hypertension.

Aged↗
PubMed1982

Hyperkinetic heart syndrome: the role of the sympathetic nervous system.

The role of the sympathetic nervous system in the hyperkinetic heart syndrome (HHS) was studied in 5 patients. Neither increased basal noradrenaline and adrenaline levels in plasma nor an increased responsiveness of the sympathetic nervous system to various stimuli could be detected in patients with HHS as compared to normal volunteers. An increased sensitivity of adrenergic receptors to catecholamines or an impaired function of the baroreceptor could not be demonstrated. A prominent role of the sympathetic nervous system cannot be postulated.

Adult↗
PubMed1993

Sympathetic nervous system disorders in man.

The sympathetic nervous system innervates most organs in the body and controls their function. A variety of disease processes, surgery or drugs can result in disordered sympathetic nerve function, which can be either localized or more generalized. Malfunction can result in either sympathetic underactivity (causing postural hypotension, impotence or anhidrosis) or overactivity (causing paroxysmal hypertension or hyperhidrosis). The investigation of sympathetic disorders depends upon the system and organs involved and should include, where relevant, investigation of the possible aetiological processes. The clinical features and management of some of the major disorders affecting the sympathetic nervous system, including the recently described syndrome of DBH deficiency, are described.

Dopamine beta-Hydroxylase↗
PubMed1995

Advances in our understanding of the role of the sympathetic nervous system in obesity.

The sympathetic nervous system (SNS) and adrenal medulla are important regulators of many physiological processes, not only concerned with the control of blood pressure, but also of metabolism. It is important to realise that activation of the SNS and adrenal medulla usually occurs selectively, rather than in an all or none manner, and that in some circumstances there can be activation of some tissues/organs and suppression of the SNS supply to others. There is evidence that the SNS affects energy expenditure, with studies in both animals and humans pointing to activation of beta-adrenoceptors as being of major importance. Thus, any alteration in the activity or effectiveness of the SNS or adrenal medulla could affect resting energy expenditure and influence the development of obesity. This review assesses the techniques available for evaluating SNS activity and considers the evidence that SNS activity is reduced in obesity. The possibility that defective SNS stimulation of energy expenditure could be altered pharmacologically is considered, and the conclusion drawn that any such approach must produce compounds which are selective for effects on metabolism, and do not cause generalized activation of the SNS.

Energy Metabolism↗