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PubMed1997

The sympathetic nervous system and the renin-angiotensin-aldosterone system in cardiovascular disease.

Both the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) have central roles in vascular adaptive processes. Stimulation of the 2 systems has been demonstrated in a range of cardiovascular disorders, including congestive heart failure and hypertension. However, elucidation regarding the interactions of the many factors involved in these 2 systems is lacking. Angiotensin-converting enzyme inhibitors have been used to reveal the contribution of some elements in the RAAS. Until relatively recently, little was known about the specific disturbances of the sympathetic nervous system in cardiovascular disease. Plasma norepinephrine levels, an indicator of sympathetic activity, have limited value because they are affected by various physiologic processes in addition to sympathetic activation. Newer approaches to the assessment of neurohormonal activity include the determination of the power content of heart-rate variability. More specific probes may lead to a better comprehension of neurohormonal physiology in health and disease and underlie future therapeutic advances targeted to prevention and treatment of specific syndromes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Diet-induced changes in sympathetic nervous system activity: possible implications for obesity and hypertension.

The sympathetic nervous system responds to changes in caloric intake; caloric restriction decreases and carbohydrate administration increases sympathetic nervous system activity in animals and man. Insulin may be a major link between changes in dietary intake and changes in central sympathetic outflow. Caloric restriction reduces, and carbohydrate administration increases blood pressure in spontaneously hypertensive rats, changes consistent with a primary effect of caloric intake on sympathetic nervous system activity. Stimulation of the sympathetic nervous system by overfeeding may contribute to the development and maintenance of hypertension in biologically-predisposed animals and man. The association of obesity and hypertension may reflect chronic overfeeding, although diet-induced changes in sympathetic nervous system activity may affect blood pressure in non-obese individuals as well.

Adolescent↗
PubMed1997

Glomerular hyperfiltration during sympathetic nervous system activation in early essential hypertension.

Glomerular hyperfiltration may be important for the development of essential hypertension. Both the renin-angiotensin system and the sympathetic nervous system influence renal hemodynamic regulation. To test the hypothesis that glomerular hyperfiltration can be unmasked by sympathetic nervous system activation, renal hemodynamics and humoral components of the renin-angiotensin system were examined at rest and during mental stress in 45 young normotensive healthy subjects and 37 young people with mild essential hypertension. GFR and renal plasma flow (RPF) were determined with inulin and para-aminohippuric acid clearance at rest and during stress. At rest, RPF, GFR, filtration fraction, plasma renin activity, angiotensin (Ang) II concentrations, and serum aldosterone values were similar in normotensive and hypertensive subjects. After stress, blood pressure increased (P < 0.01), but this was nearly identical in normotensive and hypertensive subjects (7.05 +/- 6.9 versus 7.03 +/- 4.6 mmHg, NS). The decrease in RPF (-27 +/- 54 versus -22 +/- 25 ml/min per 1.73 m2, NS) was also similar in the two groups. In contrast, the increase in GFR (+ 10.5 +/- 7.2 versus 6.08 +/- 5.7 ml/min per 1.73 m2, P < 0.001) and filtration fraction (+2.48 +/- 1.38 versus 1.82 +/- 1.49%, P < 0.05) was more marked in hypertensive than in normotensive subjects. The concomitant increase in Ang II concentrations was greater in hypertensive than in normotensive subjects (+4.6 +/- 1.0 versus -1.0 +/- 0.45 pg/ml, P < 0.001). The increase in GFR during mental stress was correlated with the increment in Ang II concentrations (r = 0.39, P < 0.001). Compared with the placebo control phase, blockade of the renin-angiotensin system with an angiotensin-converting enzyme inhibitor attenuated the increase in GFR during stress in hypertensive (8.04 +/- 5.01 versus 10.1 +/- 5.7 ml/min per 1.73 m2, P < 0.05), but not in normotensive, subjects. Even in early essential hypertension, glomerular hyperfiltration is evident during sympathetic nervous system activation, which is mediated by postglomerular vasoconstriction. This early stress-induced glomerular hyperfiltration may contribute to, or trigger, the development of essential hypertension.

Adult↗
PubMed1996

The sympathetic nervous system in hypertension and renal disease.

The sympathetic nervous system plays a critical role in the initiation and development of some types of hypertension and renal diseases. In a subgroup of essential hypertension, sympathetic overactivity is implicated in linking insulin resistance, abnormal intracellular calcium handling and high blood pressure. Endothelium-derived autocrine-paracrine factors such as endothelin and nitric oxide, have been shown to influence the sympathetic nervous system, and thus to modify blood pressure and renal function. Although the action of each endothelial factor had been separately examined, the interaction between endothelin and nitric oxide has recently been found to modulate sympathetic nerve activity in an in-vivo hypertension model. Since elevated sympathetic activity is responsible for cardiovascular complications such as myocardial infarction, it is appropriate to choose antihypertensive drugs that reduce sympathetic nerve activity and attenuate reflex activation of the sympathetic nervous system.

Animals↗
PubMed2002

[The influence of single moderate exercise on the sympathetic nervous system activity in patients with essential hypertension].

Sympathetic nervous system may play an important role in development and maintenance of hypertension. Its activity can be assessed by plasma levels of catecholamines, neuropeptide Y (NPY) and adrenergic receptor density. Hypertensive subjects may be more prone to reveal overactivity of sympathetic nervous system, for instance as a result of physical stress. The aim of the study was to determine the activity of sympathetic nervous system in young patients with newly recognized, untreated mild hypertension. INVESTIGATED GROUPS AND METHODS: The study was carried out in 22 patients (age 38.5 +/- 10.3 years) and 20 normotensive volunteers (age 38.5 +/- 8.6 years) as a control group, matched for sex. Density of alpha 2- and beta-adrenergic receptors using 3H-yohimbine and 125I-cyanopindolol respectively, total catecholamines and plasma renin activity using radioenzymatic assay, neuropeptide Y and aldosterone using radioimmunoassay were assessed in the blood taken in the supine position and after moderate bicycle ergometer exercise. RESULTS: Plasma concentration of NPY at rest did not differ between the groups, but increased significantly after exercise and was greater in hypertensive patients (p < 0.05). The density of alpha 2- and beta-adrenergic receptors at rest and after exercise in hypertensive subjects was unchanged when comparing to healthy individuals. The plasma concentrations of endogenous catecholamines, plasma renin activity and aldosterone level increase during exercise in both studied groups (p < 0.05). Aldosterone level was higher in hypertensive patients at rest (p < 0.05). There was a negative correlation between baseline aldosterone and NPY levels in hypertensive patients (r = -0.44, p < 0.05). CONCLUSION: Moderate exercise in hypertensive subjects causes the hyperactivity of sympathetic nervous system expressed as increase of NPY plasma level.

Adult↗
PubMed1990

Direct neurohumoral evidence for isolated sympathetic nervous system activation to skeletal muscle in response to cardiopulmonary baroreceptor unloading.

It has been postulated that cardiopulmonary baroreceptor unloading in humans results in nonuniform activation of the sympathetic nervous system. We reasoned that simultaneous measurements of arterial and venous norepinephrine (NE) spillover and clearance (using NE kinetics), muscle sympathetic neural activity (using microneurography), forearm blood flow (using plethysmography), and skin blood flow (using laser Doppler velocimetry) during lower body negative pressure at -15 mm Hg would isolate the location and extent of cardiopulmonary baroreceptor-mediated sympathetic nervous system activation. We exposed normal subjects (n = 8) to lower body negative pressure for 30 minutes, with measurements obtained at baseline, 5-10 minutes (EARLY), and 25-30 minutes (LATE). We found that arterial NE spillover, reflecting systemic sympathetic nervous system activation, did not increase significantly, whereas arterial NE clearance decreased significantly. In contrast, forearm venous NE spillover, reflecting skin and muscle sympathetic nervous system activation, increased by 17% and muscle sympathetic neural activity by 35% EARLY, whereas venous clearance did not change significantly. Although laser Doppler skin blood flow did not change, plethysmographic forearm blood flow (combined muscle and skin blood flow) decreased by 28%. All changes were sustained throughout 30 minutes of lower body negative pressure. Our data suggest that sympathetic vasoconstriction to muscle is greater than it is to skin in response to cardiopulmonary baroreceptor unloading. Moreover, our data suggest that reduced NE clearance in the arterial circulation is the primary mechanism by which arterial NE concentrations rise. Conversely, NE spillover appears to be the primary mechanism responsible for increasing venous NE concentrations measured from the forearm during cardiopulmonary baroreceptor unloading.

Adult↗
PubMed1990

Regulation of the level of uncoupling protein in brown adipose tissue by insulin requires the mediation of the sympathetic nervous system.

The role of the sympathetic nervous system in the regulation by insulin of the level of uncoupling protein in brown adipose tissue has been examined. The amount of uncoupling protein was substantially reduced in streptozotocin-diabetic rats, while insulin replacement to diabetic animals induced a partial restoration. Unilateral denervation of the interscapular brown fat pads also lowered the amount of uncoupling protein, and in diabetic animals inhibited the stimulation of the level of the protein by insulin replacement. Maintenance of normal uncoupling protein levels requires both insulin and the sympathetic system; regulation of the protein by insulin involves sympathetic mediation.

Adipose Tissue, Brown↗
PubMed1996

[What is the role of the sympathetic nervous system in digital vasospasms?].

The sympathetic activity is modulated by the cerebral cortex, hypothalamus, medullary vasomotor centers, and spinal cord. Finger blood flow is mainly under the control of the sympathetic nervous system. In digital vasospasm, an increased activity of the sympathetic nervous system is opposed to a local abnormality in the digital arteries. This controversy is discussed with respect to general and local control mechanisms in the peripheral blood circulation.

Cerebral Cortex↗
PubMed1988

Can plasma catecholamine levels be a useful index of sympathetic nervous system activity?

The hemodynamic responses of the sympathetic nervous system to the Valsalva maneuver were related to changes in circulating levels of catecholamines, aldosterone and plasma renin activity. Fourteen healthy normotensives (aged 27 +/- 8 years) took part. A catheter was inserted in the forearm then the subject was rested quietly (supine) for 30 mins. The Valsalva maneuver was performed (duration 40 s, intrathoracic pressure 40 mmHg) with continuous recording of supine heart rate. Blood was sampled before the maneuver (basal state) and at the bradycardic post maneuver phase for measurement of plasma noradrenaline, adrenaline, renin activity and aldosterone. In six subjects the procedure was repeated for durations of 10, 20, 30 and 40 s with a 30-min rest between each maneuver. Plasma catecholamines increased consistently (P less than 0.001) from pre- to post bradycardic phases of the maneuver. No changes in plasma renin activity or aldosterone were observed. The maximum tachycardia observed during each maneuver and the increments in catecholamine concentrations were each linearly related to the duration of straining but there was no overall correlation between the tachycardia and catecholamine concentrations. In conclusion under controlled conditions, plasma catecholamine concentrations can be useful indices of the stimulation of the sympathetic nervous system; the Valsalva maneuver does not appear to affect significantly the peripheral renin-angiotensin system; and the heart rate response to the Valsalva maneuver does not appear to be mediated solely by the sympathetic nervous system.

Adult↗
PubMed1996

[Sympathetic nervous system and endothelial function in heart failure].

Congestive heart failure is a frequent cardiovascular disease with a poor prognosis in advanced stages. Activation of neurohumoral systems such as the renin-angiotensin system and the sympathetic nervous system as well as impairment of local regulatory mechanisms (i.e. adrenoceptors, endothelial factors) play an important role in the pathogenesis and prognosis of the disease. The increase in peripheral resistance is due to imbalance of vasoconstrictors and vasodilators in favour of the vasoconstrictors and to changes in endothelial function, i.e. impaired production of nitric oxide, increased production of endothelin. Sodium and volume retention as well as the activation of the renin-angiotensin system increase preload. The sympathetic nervous system, which is known to be an independent negative prognostic factor, is activated and interacts with the renin-angiotensin system; however, up to now it is uncertain, whether these pathophysiological findings contribute to the development of congestive heart failure or if they are only secondary phenomena.

Amino Acid Sequence↗
PubMed2002

Obesity-related hypertension: role of the sympathetic nervous system, insulin, and leptin.

Heightened sympathetic nervous system activity, hyperinsulinemia, insulin resistance, and hyperleptinemia contribute to obesity-related hypertension. However, the precise mechanism and sequence of events in this pathophysiologic event have not been clarified. This review concentrates on studies helping to clarify the mechanisms of blood pressure elevation associated with weight change, concentrating on the temporal changes in neuroendocrine factors that are known to control energy metabolism and blood pressure. A better understanding of the pathophysiologic mechanisms of obesity-related hypertension may help in prevention, treatment, and slowing of the cardiovascular complications of obesity.

Blood Pressure↗
PubMed1981

Central blood pressure effects of substance P and angiotensin II: role of the sympathetic nervous system and vasopressin.

The role of the sympathetic nervous system and of arginine vasopressin (AVP) in the mediation of the central cardiovascular effects of angiotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of alpha-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH2)5VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG I responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral alpha-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in conscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.

Angiotensin II↗
PubMedDate not supplied

Abnormal stress responses in patients with diseases affecting the sympathetic nervous system.

Diseases that cause malfunction of the sympathetic nervous system provide insight into how the sympathetic nerves normally modulate responses to stress. This paper discusses insight from a number of such diseases. Transection of the cervical spinal cord leads to autonomic dysreflexia. This syndrome causes episodic hypertension in quadriplegic patients from excess sympathetic activity reflexly activated by bowel or bladder distention. These patients lack cerebral control of spinal sympathetic reflexes. Radiotherapy to the neck can destroy the arterial baroreceptors that monitor blood pressure fluctuations. Patients who lack baroreceptors have exaggerated blood pressure responses to stress. They have episodes of hypertension and hypotension that cause headaches and dizziness. Diabetics and uremics often develop a peripheral sympathetic neuropathy. They have postural hypotension and diminished blood pressure responses to stress. They are often unable to tolerate heat, exercise, or fluid deprivation. Patients with heart failure deplete sympathetic neuronal norepinephrine stores. The continual stress of heart failure diminishes their ability to respond to further stresses such as standing upright or exercising. Patients with diseases of the sympathetic nervous system illustrate that everyday occurrences such as a change in posture or ambient temperature are stresses requiring a marked change in sympathetic nervous activity. Both physical and psychological stresses elicit large initial sympathetic neuronal responses that are subsequently damped by feedback inhibition from structures such as the baroreceptors. Damage to part of these feedback loops leads to exaggerated pressor responses to stress.

Autonomic Nervous System Diseases↗
PubMed2005

Network of the sympathetic nervous system: focus on the input and output of the cervical sympathetic ganglion.

Unlike the thoracic and lumbar sympathetic nervous systems with paravertebral ganglions in individual spinal segments, the cervical sympathetic nervous system lacks segmental structures corresponding to the spinal segments and only three ganglions, namely the upper and middle cervical ganglions and the stellate ganglion, are present. Single axons have been observed in the ganglions using an anterograde-labeling method to analyze their expansion in order to investigate the relationship between the cervical sympathetic ganglions and the spinal cord in rats. Although segmental structures were not confirmed in the upper cervical ganglion, segmental structures were demonstrated in the stellate ganglion. Next, it was determined that some sympathetic preganglionic neurons, nitric oxide synthetase-positive preganglionic neurons, form dense nerve endings on the upper cervical ganglion neurons that project onto organs closely related to glandular secretion in the head and neck region. Finally, the relationship between the cell body size of upper cervical ganglion neurons and the size of the target was investigated for the three major salivary glands in rats and it was determined that no direct relationship was present.

Animals↗
PubMed1984

The involvement of the sympathetic nervous system in pain. Possible neuronal mechanisms.

The sympathetic nervous system is defined anatomically as the thoraco-lumbar autonomic nervous system with only efferent neurones projecting into the lower extremities. The afferent fibres travelling in the sympathetic nerves and supplying visceral organs are named visceral afferents. They are probably involved in visceral nociception. Some afferents in the sympathetic trunk which have been regarded by some as sympathetic afferent neurones from deep structures in the extremities in fact seem to innervate structures in the retroperitoneal space such as the vertebral column e.g. Arguments for and against the direct modulatory influence of sympathetic activity on sensory receptors in skin and skeletal muscle are discussed. It is concluded that an efferent sympathetic control of receptors in the periphery does not play a significant role in mammals. The possible involvement of the sympathetic nervous system in the pathogenesis of reflex sympathetic dystrophy is discussed in the light of recent experimental findings. The different symptoms like pain, dysregulation of blood flow and sweating, the trophic changes in skin and subcutaneous tissues are considered with respect to the complex morphological and functional changes found in primary afferent neurones, dorsal horn neurones and postganglionic vasoconstrictor neurones in animals with nerve lesions. The clinical picture of postsympathectomy pain is presented. It is proposed that the basic peripheral neuronal mechanism leading to this pain may be very much the same as it may be in different types and stages of reflex sympathetic dystrophy.

Humans↗
PubMedDate not supplied

Contribution of the sympathetic nervous system to the centrally-induced pressor action of angiotensin II in rats.

1. Angiotensin II (ANG II) may increase blood pressure by central nervous system mechanisms. The involvement of the sympathetic nervous system in the centrally-induced pressor effect of ANG II in the rat was investigated. 2. Plasma noradrenaline concentrations, measured as an index of sympathetic nervous system activity, increased after intracerebroventricular (i.c.v.) injection of pressor doses of ANG II, both in normotensive and in spontaneously hypertensive rts. 3. To assess the functional significance of this, the sympathetic nervous system was inhibited by phentolamine, reserpine, and guanethidine. In phentolamine-infused rats, low doses of i.c.v. ANG II elicited a blood pressure decrease, but at maximal pressor doses, no difference between phentolamine-treated and control rats was observed. In reserpinized rats, the central pressor effect of ANG II was greater than in controls. Guanethidine pretreatment did not affect the blood pressure response to i.c.v. injected ANG II. 4. It is concluded that the central pressor effects of ANG II are accompanied by a stimulation of the sympathetic nervous system. In the rat, this stimulation may be functionally important for the initial phase of the central pressor action. This could not be established for the maximal pressor responses.

Angiotensin II↗