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PubMed1978

[The effect of etilefrine and dihydroergotamine on sympathetic nervous system activity when standing up (author's transl)].

Systolic blood pressure, heart rate and concentrations of adrenaline, noradrenaline and dopamine as well as plasma dopamine-beta-hydroxylase (DBH) were measured in 22 subjects in recumbency and on standing up. Six subjects each had previously been given intravenously dihydroergotamine (0.5 mg) or etilefrine (0.25 mg/min) or a placebo. It was demonstrated that orthostasis leads to an increased activity of the sympathetic nervous system and the adrenal system. After administration of dihydroergotamine there was a diminished reaction of the sympathetic nervous system with an increase of venous tone which counteracted the decrease in cardiac output. Etilefrine, on the other hand, inhibited the sympatho-adrenal reaction on orthostasis and decreased the liberation of adrenaline. It acts directly via stimulation of alpha-and beta-receptors and is thus predominantly indicated if there is insufficient response of the baroreceptor reflex at its efferent limb.

Adult↗
PubMed1989

Is activation of the sympathetic nervous system beneficial or detrimental to the patient with chronic heart failure? Lessons learned from clinical trials with beta-adrenergic agonists and antagonists.

The sympathetic nervous system is markedly activated in most patients with congestive heart failure, but it is not clear whether such activity is clinically beneficial (and should be enhanced) or detrimental (and should be blocked). Some insights into this question can be gained by reviewing the results of clinical trials with beta-adrenergic agonists and antagonists. Long-term treatment with agents that stimulate the beta-receptor (prenalterol and pirbuterol) has not proved to be useful in the treatment of chronic heart failure; moreover, prolonged treatment with beta-agonists (dobutamine and pirbuterol) may adversely affect survival. Most of the studies with beta-agonists, however, have employed agents that interact nonselectively and with a high degree of intrinsic activity with both beta 1-and beta 2-receptors. It is possible that the problems that have been encountered with the use of beta-agonists could be minimized by agents that are more selective and have less intrinsic activity. Yet, such agents may actually function as beta-adrenergic antagonists (rather than agonists) in states of heightened sympathetic activity. Indeed, sustained therapy with drugs that attenuate the effects of the sympathetic nervous system (by blocking tyrosine hydroxylase or beta-adrenergic receptors) may produce hemodynamic and clinical improvement and may reduce long-term mortality in chronic heart failure. Although beta-adrenergic blockade carries important risks, these might be minimized by the use of drugs that spare myocardial and vascular beta 2-receptors or possess some intrinsic agonist activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1985

Evidence that the sympathetic nervous system does not regulate dietary thermogenesis in humans.

Overfeeding normal volunteers with either carbohydrate or a mixture of supplements for 20 days increased resting metabolic rate, but most of the excess energy was retained. There was no significant increase in urinary VMA or catecholamine excretion or plasma catecholamine concentrations during overfeeding, suggesting that there was no diffuse activation of the sympathetic nervous system. Overfeeding did not enhance the thermogenic response to norepinephrine infusion, suggesting that the increase in resting metabolic rate during overfeeding in man is not mediated by increased sensitivity to norepinephrine or by hypertrophy of brown fat. Propranolol slightly reduced postprandial resting metabolic rate during overfeeding is not mediated by increased sympathetic nervous system activity. These data are not consistent with the hypothesis that the sympathetic nervous system regulates dietary thermogenesis in man.

Adult↗
PubMed1990

Interaction of the sympathetic nervous system and electrolytes in congestive heart failure.

Congestive heart failure is characterized by both disturbances in electrolyte homeostasis and neuro-hormonal regulation. Total body potassium is reduced, and this reduction bears a modest relation to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Patients with decompensated heart failure show increases in both plasma epinephrine and plasma norepinephrine, whereas patients with chronic stable heart failure usually have an increase only in plasma norepinephrine. High levels of circulating epinephrine may contribute to the development of hypokalemia by activating skeletal muscle and liver membrane beta 2-adrenergic receptors, which in turn stimulate intracellular cyclic adenosine monophosphate to activate the membrane-bound Na+K(+)-adenosine triphosphatase pump. The net result is that potassium flux across the cell membrane from the extracellular to the intracellular space increases, setting the stage for hypokalemia and possibly serious ventricular arrhythmias. Other mechanisms that may contribute to the development of hypokalemia in heart failure include the kaliuresis brought on by excessive levels of aldosterone. Moreover, it is likely that the activity of facilitated by concomitant activation of the renin-angiotensin system. Increased sympathetic nerve activity may then release additional renin from the kidney (by way of a beta 2-adrenergic mechanism). Therefore, both the sympathetic nervous system and the adrenal medulla may interact to cause hypokalemia in patients with heart failure. Because hypokalemia is known to predispose patients to ventricular arrhythmias, it may be prudent to aggressively maintain serum potassium levels in patients with heart failure in the range of 4 to 5 mEq/liter.

Epinephrine↗
PubMed2003

Role of prostaglandin, endothelin and sympathetic nervous system on the L-NAME-induced pressor responses in spontaneously hypertensive rats.

We tested the hypothesis that in spontaneously hypertensive rat (SHR) NO produced centrally influences the resting arterial blood pressure by attenuating mechanisms involving prostaglandins, angiotensin II, endothelin and sympathetic nervous system. L-NAME (200 micro g/5 micro l), an inhibitor of NO synthase, administered intracerebroventricularly (i.c.v.) to awake and freely moving rats increased mean arterial blood pressure (MABP) in a biphasic pattern: an early transient increase within 1 min and a late prolonged response starting at 45 min and persisting for the duration of experiment (180 min). The two pressor responses involve different neurochemical mechanisms and, based on their latencies, they appear to reflect different anatomical sites of action of L-NAME. The late, but not the early pressor response, was prevented by pretreatment with chlorisondamine (2.5 mg/kg, i.v.), a ganglionic blocker, indicating its dependence on the sympathetic nervous system. Both pressor responses were abolished by i.c.v. pretreatment with indomethacin (200 micro g/5 micro l, i.c.v.), an inhibitor of cyclo-oxygenase, showing that they are mediated by prostaglandin(s). In contrast, losartan (25 micro g/5 micro l), an angiotensin II AT(1) receptor antagonist, had no effect. The initial pressor response was also attenuated by pretreatment with the endothelin ET(A)/ET(B) receptor antagonist, PD 145065 (48 micro g/2 micro l, i.c.v.). Intravenous pretreatment with another ET(A)/ET(B) receptor antagonist, L-754,142 (15 mg/kg as a bolus+15 mg/kg/h for 180 min), however, attenuated both responses to L-NAME. It is possible that L-754,142 crossed the blood-brain barrier and blocked, in addition, central ET(A)/ET(B) receptors. These studies show that NO synthesized in the brain attenuates pressor mechanisms involving prostaglandin, endothelin and sympathetic nervous system, but not angiotensin II, to modulate resting arterial blood pressure.

Acetamides↗
PubMed1990

Insulin resistance, energy balance and sympathetic nervous system activity.

Insulin resistance and hyperinsulinemia are commonly associated with hypertension in the obese. The nature of this association is obscure. An hypothesis is developed that attributes obesity-related hypertension to sympathetic stimulation. The relationship between insulin and the sympathetic nervous system (SNS) has its origins in the mediation of dietary thermogenesis. Fasting suppresses while carbohydrate and fat feeding stimulate sympathetic activity. Insulin-mediated glucose metabolism within critical central neurons links dietary intake and central sympathetic outflow. The sympathetic nervous system, in turn, contributes to changes in metabolic rate that accompany alterations in dietary intake. It is hypothesized that insulin resistance is a mechanism recruited in the obese to limit further weight gain and stabilize body mass. Insulin-mediated sympathetic stimulation is one mechanism that may restore energy balance in the obese since the obese are not resistant to the stimulatory effect of insulin on the SNS. Sympathetically mediated stimulation of the heart, vasculature and kidney contributes, in genetically predisposed individuals, to the development of hypertension. Viewed in this light, obesity-related hypertension is the unfortunate by-product of an adaptive mechanism (insulin resistance) recruited to restore energy balance in the obese. Possible implications of this formulation are discussed.

Adipose Tissue↗
PubMed1982

A model for investigating the effect of drugs on the peripheral sympathetic nervous system in man.

A model for assessing the effect of sympatholytic drugs on the peripheral sympathetic nervous system in man is described. Guanethidine, a sympatholytic drug, and the vehicle have been used to explore the model which is based on the Bier block. Sympathetic activity was assessed by measuring: (i) palmar sweating; (ii) skin temperature; (iii) radial/brachial pressure index; (iv) hand blood flow; and (v) vasoconstrictor ice response of hand blood flow. Neither the tourniquet nor the vehicle had any effect on sympathetic activity whereas guanethidine produced significant changes in skin temperature (P less than 0.05), hand blood flow (P less than 0.001) and the vasoconstrictor ice response (P less than 0.002), illustrating the usefulness of the model.

Adolescent↗
PubMed1990

Excessive sympathetic nervous system activity decreases myocardial contractility.

The objective of this study was to determine whether myocardial contractility is depressed by intense activation of the sympathetic nervous system. A massive sympathetic discharge was produced by injecting veratrine or sodium citrate into the cisterna magna of anesthetized rabbits (n = 10). Two and one-half hr later, the hearts were isolated and their left ventricular (LV) performance evaluated and compared with the LV performance of hearts isolated from control animals (n = 10). LV performance was evaluated from steady-state peak isovolumic systolic and end-diastolic pressures that were generated at various end-diastolic volumes (LV function curves). The relationship between peak LV systolic pressure (or the average peak developed LV wall stress) and LV end-diastolic volume was rotated downward (P less than 0.01) in the hearts removed from rabbits treated with veratrine or citrate. The LV end-diastolic pressure or LV end-diastolic wall stress of these hearts was not different from control at any end-diastolic volume. The diminished ability of the experimental hearts to develop systolic pressure or wall stress suggests that intense sympathetic activation depressed contractility. Severely damaged myofibers, located largely in the subendocardium, were found in these hearts. Furthermore, the depressed contractility was not related to pulmonary edema since only 2 of 10 rabbits developed edema.

Animals↗
PubMed1977

Studies on the role of sympathetic nervous system in the mechanism of essential hypertension.

In order to investigate a role of sympathetic nervous system in the mechanism of blood-pressure elevation in essential hypertension, urinary catecholamines, serum dopamine-beta-hydroxylase (DBH) activity and a pressor response to infused noradrenaline (noradrenaline response) were measured, in the patients with essential hypertension, before and 2 weeks-rest after hospitalization or following salt restriction. In addition, plasma renin activity (PRA) and water-sodium contents were determined and a correlation between these variables and noradrenaline excretion, serum DBH or noradrenaline response was observed. A blood pressure fall after hospitalization was associated with a decrease of urinary noradrenaline and serum DBH, and there was a significantly positive correlation between the changes in blood pressure and those in urinary noradrenaline or in serum DBH. A significantly adverse correlation was found between plasma volume and the amounts of urinary noradrenaline excretion. The changes in noradrenaline response was negatively correlated with those in urinary noradrenaline excretion. In addition, noradrenaline response was correlated positively with plasma volume, extracellular fluid volume and total exchangeable sodium and negatively with PRA. Following salt restriction, a fall of the blood pressure was associated with an elevation of urinary noradrenaline excretion. The patients with more marked blood pressure fall showed a higher increase of urinary noradrenaline, and a significant correlation was found between the changes in these two variables. Noradrenaline response was significantly reduced, although it was not correlated significantly with noradrenaline excretion. In these experiments, adrenaline, unlike noradrenaline, did not show any obvious changes. These findings suggested that an excessive sympathetic nerve activity caused an elevation of blood pressure in the labile type of essential hypertension. It was demonstrated that a sympathetic nervous function was dependent on sodium intake and that there exisited a close relationship between noradrenaline response and water-sodium contents or PRA.

Adolescent↗
PubMedDate not supplied

[The effect of the drug-induced activation and deprivation of the sympathetic nervous system on aldosterone receptor binding by the kidney with disturbed neurotrophic support].

The results of studies are presented on the determination of aldosterone accumulation by mineralocorticoid receptors on cytoplasm and nuclei of normal rat renal tubules as well as in disturbed neurotrophic supply of the kidney including that against the background of activation and deprivation of the sympathetic nervous system function. It was shown that a pharmacological stimulation of sympathetic nervous system potentiated functional disturbances of the renal mineralocorticoid receptor apparatus in reflex dystrophy of the kidney. A simultaneous pharmacological blockade both of neural and of humoral transmission of pathological stimuli from damaged sciatic nerve to the kidney prevented the development of these disturbances. A belief is stated that there is a possibility of using adrenoceptor blockers as means to prevent or inhibit the development of dystrophic alterations in the organism which appear under the lesion of one or other part of the nervous system.

Aldosterone↗
PubMed1997

Spontaneously hypertensive rat Y chromosome increases indexes of sympathetic nervous system activity.

Previous studies from our laboratory have demonstrated that the Y chromosome from the spontaneously hypertensive rat (SHR) is responsible for a significant portion of the elevated blood pressure and also produces an earlier pubertal rise in plasma testosterone. We performed the following studies to determine whether the SHR Y chromosome raises blood pressure by sympathetic nervous system responses as measured by adrenal chromogranin A and plasma and tissue catecholamines. Male SHR from the University of Akron colony were studied from 5 to 20 weeks of age. Blood pressure was measured by tail-cuff, tail artery cannulation, and aortic telemetry (Data Sciences); acute (air stress) and chronic (territorial colony) social stressors were compared; blood was collected for determination of plasma catecholamines; and adrenal glands were analyzed at 15 weeks for catecholamines. Rats with the SHR Y chromosome had higher blood pressure and plasma norepinephrine than those with the normotensive Wistar-Kyoto (WKY) Y chromosome. However, the SHR Y chromosome did not significantly change responsiveness to acute or chronic stressors. Phentolamine and clonidine prevented the stress responses. Adrenal chromogranin A levels were elevated 37% and 40% and adrenal norepinephrine content 29% and 100% at 4 and 10 weeks of age, respectively, in rats with an SHR Y chromosome compared with WKY. Chemical sympathectomy normalized blood pressure in all strains and significantly reduced norepinephrine (36% to 41%) in all strains except in WKY, which already had a normal blood pressure. In conclusion, the SHR Y chromosome appears to increase the chronic sympathetic nervous system. A potential mechanism could be a Y locus that influences chronic sympathetic nervous system activity, which may reinforce neurohumoral factors and structural components of the vessel wall, accelerating the development of hypertension.

Adrenal Glands↗
PubMed2000

Responses of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis to interleukin-6: a pilot study in fibromyalgia.

OBJECTIVE: To determine whether deficient activity of the hypothalamic corticotropin-releasing hormone (CRH) neuron, which stimulates the hypothalamic-pituitary-adrenal (HPA) axis and the central control nuclei of the sympathetic nervous system and inhibits ascending pain pathways, may be pathogenic in patients with fibromyalgia (FM). METHODS: We administered interleukin-6 (IL-6; 3 microg/kg of body weight subcutaneously), a cytokine capable of stimulating hypothalamic CRH release, and measured plasma levels of adrenocorticotropic hormone (ACTH), cortisol, and catecholamines and their metabolites and precursors. Thirteen female FM patients and 8 age- and body mass index-matched female controls were studied. The diagnosis of FM was made according to American College of Rheumatology criteria. Tender points were quantitated by pressure algometry. All subjects had HPA axis studies. Seven FM patients and 7 controls also had catecholamine measurements. RESULTS: After IL-6 injection, delayed ACTH release was evident in the FM patients, with peak levels at 96.9 +/- 6.0 minutes (mean +/- SEM; control peak 68.6 +/- 10.3 minutes; P = 0.02). Plasma cortisol responses to IL-6 did not differ significantly between patients and controls. Basal norepinephrine (NE) levels were higher in the FM patients than in the controls. While a small, although not significant, rise in NE levels occurred after IL-6 injection in the controls, NE levels dramatically increased over basal levels in the FM patients between 60 and 180 minutes after IL-6 injection. Both peak NE levels (mean +/- SEM 537.6 +/- 82.3 versus 254.3 +/- 41.6 pg/ml; P = 0.0001) and time-integrated NE responses (93.2 +/- 16.6 pg/ml x minutes(-3) versus 52.2 +/- 5.7 pg/ml x minutes(-3); P = 0.038) were greater in FM patients than in controls. Heart rate was increased by IL-6 injection in FM patients and controls, but rose to significantly higher levels in the FM patients from 30 minutes to 180 minutes after IL-6 injection (P < 0.03). CONCLUSION: Exaggerated NE responses and heart rate increases, as well as delayed ACTH release, were observed among female FM patients compared with age-matched female controls. Delayed ACTH release after IL-6 administration in FM is consistent with a defect in hypothalamic CRH neuronal function. Exaggerated NE release may reflect abnormal regulation of the sympathetic nervous system, perhaps secondary to chronically deficient hypothalamic CRH. The excessive heart rate response after IL-6 injection in FM patients may be unrelated to the increase in NE, or it may reflect an alteration in the sensitivity of cardiac beta-adrenoceptors to NE. These responses to a physiologic stressor support the notion that FM may represent a primary disorder of the stress system.

Adrenocorticotropic Hormone↗
PubMed1990

Pseudorabies virus: a highly specific transneuronal cell body marker in the sympathetic nervous system.

The present report presents a series of experiments using Bartha's K strain of pseudorabies virus (PRV) designed to test the specificity of this virus as a retrograde transneuronal marker in the sympathetic nervous system of rats. Three experiments were performed. First, an injection of PRV was made in the anterior chamber of the eye, followed 24 hr later by an injection of WGA-HRP. PRV infected neurons in the superior cervical ganglion (SCG) always contained WGA-HRP. This dual labeling of SCG neurons suggests that the PRV cell body labeling does not nonspecifically infect nearby neurons. Second, after PRV injections into the pinna or eye, a specific segmental distribution of the transneuronal cell body labeling occurred in the intermediolateral cell column and related spinal areas. After eye injections, the majority of transneuronally labeled neurons were in the T1-T3 segments. After pinna injections, the majority of labeled cells were in the T2-T5 segments. Since the SCG cells innervating these 2 end organs lie in close proximity to each other within the ganglion, these results suggest that a specific transfer of the virus to the preganglionic neurons occurred, possibly via a transsynaptic mechanism. Third, virally infected glial cells were rarely found in the SCG or spinal cord. In summary, Bartha's K strain of PRV is a specific transneuronal retrograde grader marker in the sympathetic nervous system.

Animals↗
PubMed1986

Mechanisms of causalgia and related clinical conditions. The role of the central and of the sympathetic nervous systems.

The definition of causalgia as a pain state following peripheral nerve injury has been accepted since the term was introduced by Weir Mitchell over a century ago. In the present paper, problems of nomenclature and nosology are discussed, and attention is drawn to the fact that the same clinical features can occur spontaneously, in nontraumatic nerve lesions, in the absence of a part as in phantom limb states, and in diseases confined to the central nervous system. Attention is also drawn to the lack of correlation of pain with the effects mediated by catecholamines in the sympathetic nervous system and with the response to sympathetic blockade. Concerning mechanisms, a number of peripheral mechanisms have been postulated. These are reviewed, and while they might be correct when causalgia arises from peripheral nerve damage, they cannot provide adequate explanation for at least some instances of causalgia. The relevance of the neuroma as a model for chronic pain in general, and causalgia, is questioned. Also questioned is the view that causalgia is a state that depends on peripheral involvement of the sympathetic nerve supply. Certain authors in the past considered that the central nervous system (CNS) played an important part in causalgia, and current evidence supporting this view is assessed. Involvement of the CNS is suggested by the development of causalgia in diseases confined to the CNS and in phantom pain states; the unusual distribution of pain sometimes experienced; the paradoxical development of widespread pain that can occur after damage to the sympathetic nervous system; the effects of peripheral sympathetic blockade even when the cause lies centrally; and central interactions with motor, sensory and psychological phenomena. Reservations concerning the role of catecholamines in causalgia are outlined, and the possibility is considered that nonadrenergic substances may be implicated.

Adult↗
PubMed1995

Central command neurons of the sympathetic nervous system: basis of the fight-or-flight response.

During stress, the activity of the sympathetic nervous system is changed in a global fashion, leading to an increase in cardiovascular function and a release of adrenal catecholamines. This response is thought to be regulated by a common set of brain neurons that provide a dual input to the sympathetic preganglionic neurons regulating cardiac and adrenal medullary functions. By using a double-virus transneuronal labeling technique, the existence of such a set of central autonomic neurons in the hypothalamus and brainstem was demonstrated. These neurons innervate both of the sympathetic outflow systems and likely function in circumstances where parallel sympathetic processing occurs, such as in the fight-or-flight response.

Adrenal Glands↗
PubMed1990

Noninvasive evaluation of sympathetic nervous system in human heart by positron emission tomography.

The noninvasive functional characterization of the cardiac sympathetic nervous system by imaging techniques may provide important pathophysiological information in various cardiac disease states. Hydroxyephedrine labeled with carbon 11 has been developed as a new catecholamine analogue to be used in the in vivo evaluation of presynaptic adrenergic nerve terminals by positron emission tomography (PET). To determine the feasibility of this imaging approach in the human heart, six normal volunteers and five patients with recent cardiac transplants underwent dynamic PET imaging after intravenous injection of 20 mCi [11C]hydroxyephedrine. Blood and myocardial tracer kinetics were assessed using a regions-of-interest approach. In normal volunteers, blood 11C activity cleared rapidly, whereas myocardium retained 11C activity with a long tissue half-life. Relative tracer retention in the myocardium averaged 79 +/- 31% of peak activity at 60 minutes after tracer injection. The heart-to-blood 11C activity ratio exceeded 6:1 as soon as 30 minutes after tracer injection, yielding excellent image quality. Little regional variation of tracer retention was observed, indicating homogeneous sympathetic innervation throughout the left ventricle. In the transplant recipients, myocardial [11C]hydroxyephedrine retention at 60 minutes was significantly less (-82%) than that of normal volunteers, indicating only little non-neuronal binding of the tracer in the denervated human heart. Thus, [11C]hydroxyephedrine, in combination with dynamic PET imaging, allows the noninvasive delineation of myocardial adrenergic nerve terminals. Tracer kinetic modeling may permit quantitative assessment of myocardial catecholamine uptake, which will in turn provide insights into the effects of various disease processes on the neuronal integrity of the heart.

Adult↗