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At least 127 records · Page 7Linked to original sources
PubMed1999

Pressor and renal vasoconstrictor responses to acute systemic nitric oxide synthesis inhibition are independent of the sympathetic nervous system and angiotensin II.

Acute systemic, nonselective nitric oxide synthesis inhibition (NOSI) causes a marked pressor and renal vasoconstrictor response in the normal conscious chronically catheterized rat. The present studies directly address the question of how these vasoconstrictor responses are related to the combined vasoconstrictor activities of the sympathetic nervous system and angiotensin II. When the alpha adrenoceptors are blocked (with prazosin) the pressor and renal hemodynamic responses to NOSI are unaffected. Combined alpha adrenoceptor and angiotensin II receptor blockade at the same time as NOSI results in no net change in blood pressure while leaving the renal vasoconstrictor response intact. However, when the NOSI is delayed, a substantial and unblunted pressor response is seen. In contrast to the vasoconstrictor responses, the natriuretic and diuretic responses to acute NOSI are prevented by simultaneous alpha adrenoceptor blockade alone and combined with angiotensin II receptor blockade. These findings suggest that the hemodynamic actions of acute NOSI in the unstressed rat are independent of the sympathetic nervous system and angiotensin II. In contrast, the natriuretic/diuretic response to acute NOSI is apparently partly the result of some interaction with the sympathetic nervous system, not, as we had previously suggested, exclusively the result of a pressure natriuresis.

Adrenergic alpha-Antagonists↗
PubMed2000

Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury.

Spinal cord injury (SCI) with resultant quadriplegia or high paraplegia is associated with significant dysfunction of the sympathetic nervous system. This alteration of sympathetic nervous system activity occurs as a consequence of loss of supraspinal control of the sympathetic nervous system and is further complicated by at least three subsequent phenomena that occur below the level of SCI: reduced overall sympathetic activity, morphologic changes in sympathetic preganglionic neurons, and peripheral alpha-adrenoceptor hyperresponsiveness. Reduced sympathetic activity below the level of SCI appears to result in orthostatic hypotension, low resting blood pressure, loss of diurnal fluctuation of blood pressure, reflex bradycardia, and, rarely, cardiac arrest. Peripheral alpha-adrenoceptor hyperresponsiveness likely accounts for some, if not the majority, of the excessive pressor response in autonomic dysreflexia and may also contribute to decreased blood flow in the peripheral microcirculation, potentially increasing susceptibility to pressure sores. What has yet to be established is whether this alpha-adrenoceptor hyperresponsiveness is a consequence of receptor hypersensitivity or a failure of presynaptic reuptake of noradrenaline at the receptor level. Better understanding of the pathophysiology of sympathetic nervous system dysfunction after high-level SCI should allow development of more effective measures to manage clinical complications.

Autonomic Dysreflexia↗
PubMed1991

Influence of the sympathetic nervous system as well as trigeminal sensory fibres on rat dural mast cells.

The dura mater has attracted considerable attention as an exquisitely sensitive tissue implicated as playing a role in various cephalalgias including vascular headache. Because of the potential clinical impact of the relationship/interaction of neural elements and mast cells the influence of sensory and autonomic nerve fibres on mast cells of the rat dura mater was studied. The trigeminal or superior cervical ganglion was electrically stimulated and the mast cells were examined. Wholemount supratentorial dural preparations were stained using berberine sulphate and the number of mast cells with intact vs dispersed granules counted. Unilateral stimulation of either ganglia resulted in a statistically significant increase in the percentage of mast cells with dispersed granules ipsilateral to the side of stimulation. These results support our idea that in addition to the trigeminal system the sympathetic nervous system must be considered as playing a role in the oedema pathophysiology of vascular headache.

Animals↗
PubMed1993

Modulation of the jaw jerk reflex by the sympathetic nervous system.

The effect of sympathetic stimulation on the jaw jerk reflex has been studied in precollicular decerebrate rabbits. This reflex was elicited by a downward mandibular movement applied to the lower jaw through a servo controlled puller. Unilateral stimulation of the cervical sympathetic nerve at 10/s consistently induced a decrease in the JJR, i.e. a marked reduction of the EMG activity in the ipsilateral masseter muscle, accompanied by a 30-40% decrease in the reflexly developed force. In these trials EMG of the contralateral muscle, recorded as control, was not significantly affected. Bilateral stimulation of cervical sympathetic nerve strongly reduced or suppressed the EMG activity in both sides and produced a parallel decrease in the developed force which reached values ranging from 12.5% to 37.0% of controls (with an average of 28.9% +/- 8.9, S.D.). The effect of sympathetic stimulation was also tested on the contraction of the masseter muscle elicited by direct electrical stimulation. Sympathetic activation induced a modest increase in both amplitude and duration of muscle twitch, thus showing that the reduction in the reflex response can not be attributed to an action exerted by the adrenergic mediator on the muscular contraction. All these effects were almost completely abolished by the blockade of alpha-adrenergic receptors. They were proved not to be secondary to the sympathetically-induced vasomotor changes. Therefore the marked JJR reduction produced by activation of the sympathetic nervous system is suggested to be due to the sympathetically-induced decrease in neuromuscular spindle sensitivity to muscle length changes, previously reported.

Adrenergic alpha-Antagonists↗
PubMed2001

Sympathetic nervous system and experimental diabetes: role of adrenal medullary hormones.

The sympathetic nervous system is of major importance in the regulation of various physiological functions. The present review discusses the mechanisms which control glucose homeostasis and the role of the sympathetic nervous system in experimental diabetes with special emphasis on the role of adrenal medullary hormones, over-activity of the sympathetic nervous system and its relationship to hypertension in the diabetic state and the effect of stress. The chapter also reviews the ability of various drugs and pharmacological agents to produce hyperglycemia in experimental animals and how this information can be used in screening new chemical entities and in differentiating the mode of action of these agents.

Adrenal Medulla↗
PubMed1980

Sympathetic nervous system activity during sodium restriction in essential hypertension.

Sympathetic nervous system activity was studied in 38 patients with essential hypertension during high- and low-sodium diets. Salt restriction was associated with a modest (6 mmHg) decline in mean arterial pressure, while the urinary excretion of catecholamines, metanephrines, and vanillylmandelic acid increased significantly. Plasma renin activity also increased. It is concluded that short-term low-sodium diet therapy for essential hypertension results in only small decrements in mean arterial pressure and may be limited in hypotensive effect by activation of the sympathetic nervous system. Support is offered for the rationale of sympatholytic drug therapy as an initial step in the management of hypertensive patients requiring arterial pressure reductions greater than those afforded by diet alone.

Adult↗
PubMed1990

Role of the sympathetic nervous system in the genesis of ventricular arrhythmia.

Activation of the sympathetic nervous system is an important factor in the genesis of ventricular arrhythmias in patients with impaired ventricular function. Such patients have an appropriate substrate that is capable of generating rhythm abnormalities, which may be related to enhanced automaticity, triggered automaticity, and reentrant mechanisms; all three mechanisms are markedly potentiated by the action of catecholamines. Additionally, the sympathetic nervous system can provoke the development of hypokalemia and ischemia (which can independently lead to the occurrence of rhythm disturbances), and catecholamines may negate the beneficial electrophysiological actions of antiarrhythmic drugs. A substantial amount of experimental data implicates the sympathetic nervous system as a potent stimulus for ventricular tachyarrhythmias and sudden cardiac death, especially in the setting of myocardial ischemia. Two important mechanisms that have been identified include 1) enhanced sympathetic outflow from the central nervous system and 2) nonuniform myocardial denervation resulting in beta-receptor up-regulation and catecholamine hypersensitivity in the infarct zone. Disruption of sympathetic neural innervation of the heart and the use of beta-blocking agents may reduce the occurrence of sudden death and improve survival in animal models of arrhythmias and in some subsets of patients, including those with the long QT syndrome, a recent myocardial infarction, and perhaps those with a cardiomyopathy. The mechanism of this beneficial effect remains to be defined.

Adrenergic beta-Antagonists↗
PubMed1984

Vasodilative effect of hydralazine in awake dogs: the roles of prostaglandins and the sympathetic nervous system.

The relative roles of prostaglandins and the sympathetic nervous system in mediating the hypotensive effects of hydralazine were studied in awake dogs with and without pretreatment with indomethacin, propranolol, and phentolamine. In normal dogs, mean aortic pressure decreased 23 +/- 4 mm Hg after administration of hydralazine (cumulative dose of 0.8 mg/kg). This hypotensive effect of hydralazine was potentiated by phentolamine but was abolished by propranolol. Indomethacin caused a paradoxic pressor response (11 +/- 3 mm Hg) to hydralazine, which also was abolished by addition of phentolamine. Hydralazine produced vasodilation in the coronary, skeletal muscle (quadriceps), splanchnic, and renal circulations in normal dogs. The increase in coronary blood flow was associated with increased cardiac oxygen consumption and narrowed arteriovenous oxygen difference across the heart. Propranolol reduced the increases in cardiac oxygen consumption and coronary blood flow, but only indomethacin abolished the narrowed arteriovenous oxygen difference, suggesting that the increase in coronary blood flow was related to both the increased cardiac oxygen demand and prostaglandin-mediated active coronary vasodilation. The decrease in skeletal muscle vascular resistance after hydralazine was abolished by propranolol. Skeletal muscle vascular resistance actually increased after administration of hydralazine in dogs pretreated with both propranolol and indomethacin. These effects were blocked by the addition of phentolamine. Unlike the normal response, renal and splanchnic vascular resistances increased after administration of hydralazine in dogs pretreated with indomethacin. The splanchnic vasoconstriction was abolished by phentolamine, but the renal vascular change was affected by neither phentolamine nor propranolol. The results indicate that hydralazine does not produce uniform vasodilation in all organs and that the cardiovascular actions of hydralazine involve both prostaglandins and the sympathetic nervous system.

Animals↗
PubMed1995

Sympathetic nervous system: contribution to human hypertension and related cardiovascular diseases.

Sympathetic nervous system activation has been documented in several cardiovascular disorders. In some, characterized by cardiac failure and portal hypertension accompanying hepatic cirrhosis, the sympathetic nervous stimulation is reflex and, to some extent, compensatory but has adverse consequences. For example, in cardiac failure, the sympathetic nerves of the heart are preferentially stimulated, providing adrenergic support to the failing myocardium but at the probable cost of arrhythmogenesis and progressive myocardial deterioration. The sympathetic activation present in patients with essential hypertension, which involves the sympathetic outflows to skeletal muscle, heart, and kidneys and is seen particularly in younger patients, differs from these examples in that the sympathetic nervous stimulation is apparently not reflex and the primary cause is unknown. There is, however, evidence that activation of forebrain pressor noradrenergic nuclei may be of importance as an underlying central nervous system mechanism. This sympathetic nervous stimulation in patients with essential hypertension, in addition to initiating the blood pressure elevation, may also contribute to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidemia, with neural vasoconstriction having metabolic consequences, impairing glucose delivery and causing insulin resistance in muscle, and retarding postprandial clearing of lipids in liver. Trophic effects of sympathetic activation on cardiovascular growth are claimed but have yet to be demonstrated conclusively in humans.

Cardiovascular Diseases↗
PubMed1991

[Role of the sympathetic nervous system in heart failure].

An increased activity of the sympathetic nervous system has been regarded as a sensible compensatory mechanism in heart failure. Further stimulation of this system by therapeutic interventions has proven useful in the situation of acute heart failure; however, the contractile reserve elicited by beta-stimulation is markedly reduced. By long-term stimulation of the sympathetic nervous system in the treatment of chronic heart failure mostly unfavorable effects are evoked, i.e.: 1) An increase in impedance for the failing heart by stimulation of peripheral alpha 1-adrenoreceptors. 2) An increase in myocardial oxygen consumption which causes further deterioration of the energy balance in the failing heart. 3) A fall in serum potassium concentration by stimulation of beta 2-receptors combined with a reduction of the fibrillation threshold favor the genesis of malignant arrhythmias. 4) Stimulation of myocardial alpha 1-adrenoreceptors may lead to a de-differentiation with a preferential synthesis of fetal myosins. Because of a reduced rate of calcium removal during diastole, increases in heart rate lead to an elevated myocardial stiffness. An increased sympathetic activity in patients with heart failure represents an independent marker of a reduced life expectancy. Interventions that either cause a reduction in sympathetic activity or which protect the heart from high catecholamine concentrations in heart failure are associated with an improvement of survival and quality of life.

Heart Failure↗
PubMed1979

The involvement of the sympathetic nervous system in tetanus.

Besides the characteristic disturbances of the motor nervous system symptoms indicating an overactivity of the sympathetic nervous system can complicate the course of severe cases of tetanus. These symptoms include fluctuating tachycardia and hypertension, electrocardiographic changes, sweating, constipation with development of paralytic ileus and metabolic disorders. These symptoms are comparable to these developing in patients with phaeochromocytoma. Elevated catecholamine levels in plasma and urine have been found in several patients with tetanus who developed these symptoms. The prolonged over-activity of the sympathetic nervous system is thought to contribute to the still considerably high mortality rate. Myocardial lesions observed at necropsy are comparable to those found in patients dying of phaeochromocytoma. These lesions are suggested to be associated with sudden death from arrhythmias or cardiac failure in patients with tetanus. For the protection of the organism against the overactivity of the sympathetic nervous system a treatment using the combination of beta-adrenergic receptor blocking agents and adrenergic neuron blocking agents has been introduced. A reduction of the mortality rate was achievable by this treatment. Experimental evidence is accumulating that the tetanus toxin affects not only the motor, but also the sympathetic and sensory neurons.

Adrenergic beta-Antagonists↗
PubMed1997

Effect of centrally administered endothelin agonists on systemic and regional blood circulation in the rat: role of sympathetic nervous system.

The aims of the present study were to determine (1) the hypotensive and regional circulatory effects of centrally administered endothelin (ET) ETA and ETB agonists, and (2) the role of the sympathetic nervous system in the mediation of hypotensive effects due to centrally administered ET-1. The systemic haemodynamics and regional blood circulation in urethane anaesthetized rats following intracerebroventricular (i.c.v.) administration of ET-1, ET-2, SRT6b, ET-3 and SRT6c (10, 30 and 90 ng) were determined by a radioactive microsphere technique. The effect of centrally administered ET-1 on sympathetic nerve activity was also analysed. Systemic haemodynamics and regional blood circulation were determined before (baseline) and 30 min after administration of ET agonists. Cumulative administration of three doses of saline (5 microliters, i.c.v. at 30 min intervals) did not produce any significant cardiovascular effects. ET-1, ET-2 and SRT6b produced a decrease in blood pressure (51%, 47% and 41%, respectively) along with a decrease in cardiac output (58%, 60% and 45%, respectively) and stroke volume. Heart rate and total peripheral resistance were not affected. ET-1, ET-2 and SRT6b also produced a significant reduction in blood flow to the brain, kidneys, heart, portal, mesentery and pancreas, gastrointestinal tract (GIT) and musculoskeletal system. The effect of ET-2 on the cardiovascular system was less intense in comparison with ET-1 and SRT6b. Centrally administered specific ETB receptor agonists ET-3 and SRT6c did not produce any change in systemic haemodynamics and regional blood flow. Centrally administered ET-1 (90 ng) produced a significant decrease (61%) in sympathetic nerve activity 30 min after drug administration, along with a fall in blood pressure. It is concluded that centrally administered ETA agonists produce significant cardiovascular effects mediating through the sympathetic nervous system.

Animals↗
PubMed1993

[Tonus of the sympathetic nervous system].

According to some investigators, tonus of sympathetic nervous system is not observed at all or marked a little, according to others--it is marked well. Tonus of sympathetic nerve has not been discovered at all in our experiments. The experiments have been made on narcotized and non-narcotized pigeons, guinea pigs, rats and dogs. The frequency of heart beats is regulated by n. vagus and humoral substances in rest.

Animals↗
PubMed1989

Sympathetic nervous system and hypertension. Therapeutic perspectives.

The sympathetic nervous system has a key role in the physiological regulation of the circulation and may also mediate some of the factors that cause or sustain clinical hypertension. Most classes of antihypertensive drugs produce at least part of their effects by inhibitory actions on the sympathetic pathways. The centrally acting agents and the peripheral alpha-adrenergic blockers are the most specific currently used sympathetic inhibitors. The available alpha-blockers, prazosin and terazosin, effectively reduce blood pressure when used as monotherapy or in combination with other antihypertensive drugs. When given once daily, the actions of terazosin persist throughout the full 24-hour period, including the important midmorning hours when there may be heightened sympathetic activity. The incidence of symptomatic adverse effects with the alpha-blockers is low. Because they specifically block peripheral alpha-receptor-mediated vasoconstriction, the alpha-blockers decrease total peripheral resistance at rest and do not antagonize the appropriate vasodilatory responses to exercise. They maintain or increase blood flow in regional circulations; cerebral blood flow in elderly patients is unchanged despite significant decreases in systemic blood pressure. In contrast to other drug classes that can adversely affect the lipid profile, the alpha-blockers slightly decrease total cholesterol concentrations. Recent studies also have shown that terazosin and prazosin can promote decreases in echocardiographically measured left ventricular wall thickness and muscle mass in hypertensive patients with left ventricular hypertrophy. Thus, this type of sympathetic blockade not only produces antihypertensive effects, but additionally may have a beneficial impact upon other cardiovascular risk factors.

Adrenergic alpha-Antagonists↗
PubMed1978

The influence of the sympathetic nervous system on capillary permeability.

1. The influence of the sympathetic nervous system on capillary permeability was studied in cats. The dye penetration from the blood through the synovial membrane was tested by perfusing the two knee joints, one of which was deprived of its sympathetic nerve supply by unilateral lumbosacral sympathectomy. 2. In confirmation of previous experiments, it was found in a great majority of experiments that, in spite of marked vasodilatation, the dye excretion was considerably reduced on the sympathectomised side. 3. A large amount of experimental evidence, supporting directly or indirectly, my views, has been reviewed. 4. A permeability factor under the influence of the sympathetic nervous system has been postulated; its character and mechanism is still unknown. 5. Further unpublished experiments seem to support the view that increased blood supply is associated with decreased vascular permeability.

Animals↗
PubMed1991

[Activity of the sympathetic nervous system and of the renin-angiotensin system in the acute stage of myocardial infarction].

We studied sympathetic and renin-angiotensin systems activity in a series of 175 patients suffering from acute myocardial infarction. These two systems were both overactivated especially in the cases complicated by hemodynamically documented left heart failure. The response of these systems to acute heart failure was in the same range for patients younger or older than 65 years and the witness (norepinephrine and plasma renin levels) of sympathetic and renin-angiotensin activities were good independent prognostic factors of in-hospital mortality.

Acute Disease↗
PubMed1997

Interactions between angiotensin II and the sympathetic nervous system in the the long-term control of arterial pressure.

1. The role of the renin-angiotensin system in long-term control of sympathetic activity and arterial pressure is reviewed. 2. There is evidence that favours a necessary role for the sympathetic nervous system in long-term arterial pressure regulation. First, appropriate changes in sympathetic activity appear to be produced in response to chronic changes in blood volume or blood pressure. Second, prevention of the normal homeostatic decrease in sympathetic activity in response to an increase in sodium intake produces hypertension. 3. Long-term changes in sympathetic activity cannot be mediated by the baroreceptor reflex, because it adapts to sustained changes in pressure. Therefore, an hypothesis is presented that evokes a key role for angiotensin II (AngII) in determining the chronic level of sympathetic activity. The key feature of this model is that the role of AngII is non-adaptive: chronic changes in extracellular fluid volume produce sustained reciprocal changes in AngII, and long-term increases in AngII produce sustained increases in sympathetic activity. 4. Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension.

Angiotensin II↗