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Sympathetic nervous system activation

The regulation of the total peripheral resistance also involves the complex interactions of several mechanisms. These include baroreflexes and sympathetic nervous system activity response to neurohumoral substances and endothelial factors myogenic adjustments at the cellular level, some mediated by ion channels and events at the cellular membrane and intercellular events mediated by receptors and mechanisms for signal transduction. As examples of some of these mechanisms, there are two major neural reflex arcs (Fig. 1). Baroreflexes are derived from high-pressure barorecep-tors in the aortic arch and carotid sinus and low-pressure cardiopulmonary baroreceptors in ventricles and atria. These receptors respond to stretch (high pressure) or... [Pg.273]

Signs and symptoms of sympathetic nervous system activity are invariably found in MH. Levels of catecholamines are markedly increased in MH. Whether activation of the sympathetic nervous system is a primary or a secondary response in the syndrome has not been fully elucidated. Gronert reported that stress-induced sympathetic hyperactivity can initiate a malignant hyperthermic episode in susceptible swine without a triggering agent. Stress-induced MH in humans has been inferred because susceptible families have been shown to have an increased incidence of sudden death. Gronert s reasons that activation of the sympathetic... [Pg.402]

Pheochromocytoma A tumor arising from chromaffin cells, most commonly found in the adrenal medulla. The tumor causes the adrenal medulla to hypersecrete epinephrine and norepinephrine, resulting in hypertension and other signs and symptoms of excessive sympathetic nervous system activity. The tumor is usually benign but may occasionally be cancerous. [Pg.1574]

Veith, R. C., Lewis, N., Linares, O. A. etal. (1994). Sympathetic nervous system activity in major depression. Arch. Gen. Psychiatry, 51,411-22. [Pg.85]

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. [Pg.95]

Nesiritide is manufactured using recombinant techniques and is identical to the endogenous B-type natriuretic peptide secreted by the ventricular myocardium in response to volume overload. Consequently, nesiritide mimics the vasodilatory and natriuretic actions of the endogenous peptide, resulting in venous and arterial vasodilation increases in cardiac output natriuresis and diuresis and decreased cardiac filling pressures, sympathetic nervous system activity, and renin-angiotensin-aldosterone system activity. [Pg.108]

SYMPATHETIC NERVOUS SYSTEM ACTIVITY + ANTIDIURETIC HORMONE (ADH), Water retention + Blood pressure increase... [Pg.157]

E. The effect of ganglionic blockade depends upon the predominant autonomic tone exerted within various organ systems. Since the activity of the parasympathetic nervous system predominates in the eye, the effect of ganglionic blockade is mydriasis, not miosis. Similarly, stimulation of the genital tract and urinary retention would be decreased. Since sympathetic nervous system activity predominates in blood vessels and the ventricles, vasodilation and a decreased cardiac output would follow ganglionic blockade. [Pg.147]

Adrenoceptor blockade is a rational approach to the treatment of angina pectoris, since an increase in sympathetic nervous system activity is a common feature in acute anginal attacks. Based on their ability to reduce oxygen demand, all (3-blockers tested so far have also been shown to be effective in the treatment of second-... [Pg.200]

In most forms of shock, intense vasoconstriction, mediated by reflex sympathetic nervous system activation, is present. Indeed, efforts aimed at reducing rather than increasing peripheral resistance may be more fruitful to improve cerebral, coronary, and renal perfusion. A decision to use vasoconstrictors or vasodilators is best made on the basis of information about the underlying cause, which may require invasive monitoring. [Pg.189]

In addition to its effects on cardiac contractility, digitalis has a direct inhibitory effect on sympathetic nervous system activity.37,60 This effect is beneficial because it decreases stress on the failing heart by decreasing excessive sympathetic stimulation of the heart and peripheral vasculature2. Therapeutic levels of digitalis likewise stabilize heart rate and slow impulse conduc-... [Pg.337]

There is emerging evidence that OSA may be a pro-inflammatory disorder with elevated circulating cytokines [60]. Abdominal visceral fat is a major reservoir of cytokines, and obesity is a leading risk factor for the presence of OSA [60], The mechanism(s) whereby pro-inflammatory cytokines are elevated in OSA is not fully elucidated, but may be related to the excessive sympathetic nervous system activation notable in OSA. Tumor necrosis factor (TNF)-a and interleukin (IL)-6 levels are elevated in OSA [61,62] and the circadian rhythm of TNF-a is disrupted in OSA [63]. IL-6 levels are higher again in OSA patients with systemic hypertension compared to normotensive apneics [60], IL-6 levels return to normal in OSA patients treated effectively with CPAP [64]. Other mediators of inflammation elevated in OSA include intercellular adhesion molecule-1 and C-reactive protein, the latter being synthesized primarily in hepatocytes in response to IL-6 [60], The presence of these and other pro-inflammatory cytokines may link to the increased prevalence of cardiovascular morbidity in OSA. [Pg.28]

Figure 9.3. Autonomic nervouse system showing typical panic responses in phobia and reflecting increased sympathetic nervous system activity. Figure 9.3. Autonomic nervouse system showing typical panic responses in phobia and reflecting increased sympathetic nervous system activity.
Angiotensin II is an octapeptide, which was initially described as a potent vasoconstrictor agent. However, its functions have since been expanded to include regulation of cell growth, inflammation, electrolyte and water balance, hormone secretion, sympathetic nervous system activity, differentiation, and apoptosis. The discovery that it is produced both systemically and locally was instrumental in establishing a pivotal role for the peptide in several disease states, including hypertension, coronary heart disease, myocarditis, congestive heart failure, atherosclerosis, and nephrosclerosis. [Pg.117]

Increased sympathetic nervous system activity. There is evidence of elevated plasma concentrations of adrenaline and noradrenaline in vitamin Bg-deficient animals. [Pg.265]

Psilocybin, the psychoactive principle in psilocybe mushrooms, is fairly rapidly changed into psilocin after oral ingestion, making the latter the active hallucinogen. Psilocin is 4-hydroxy DMT, i.e., DMT with an additional hydroxy molecule at the 4-position. Physiologically, psilocin (and psilocybin and the mushrooms) produces moderately intense sympathetic nervous system activation within 30 minutes of... [Pg.26]

The authors suggested that torsade de pointes induced by intravenous amiodarone depended on heart rate during a bout of bradycardia, while that after oral amiodarone depended on increased sympathetic nervous system activity, and that therefore different electrophysiological mechanisms had been at play. However, it is by no means clear from their description of this case that that was so. They did not report plasma concentrations of amiodarone or desethylamiodarone, its active metabolite. [Pg.163]

Disulfiram in a dose of 250-300 mg/day does not affect pulse rate, blood pressure, or plasma noradrenaline concentrations, but 500 mg/day causes an increase in plasma noradrenaline, increased systolic blood pressure both recumbent and erect, and an increased erect pulse rate. The raised blood pressure does not reach hypertensive values, but the results suggest increased sympathetic nervous system activity in patients who take disulfiram. Caution should therefore be exercised in using disulfiram in hypertensive patients. Close monitoring of blood pressure is advised, and the dose of disulfiram should preferably be reduced to 250 mg/day (5). [Pg.1149]

Lake CR, Major LF, Ziegler MG, Kopin IJ. Increased sympathetic nervous system activity in alcoholic patients treated with disulfiram. Am J Psychiatry 1977 134(12) 1411-14. [Pg.1151]


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See also in sourсe #XX -- [ Pg.103 ]

See also in sourсe #XX -- [ Pg.36 ]




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