Antihypertensive Drugs and Sympathetic Nervous System

Abstract

Several studies have demonstrated that essential hypertension is accompanied by sympathetic activation, which contributes to blood pressure elevation. Sympathetic activation also has adverse consequences in hypertensive patients beyond initiating blood pressure elevation. There is evidence that neural vasoconstriction has metabolic effects in skeletal muscle, impairing glucose delivery to muscles. In the liver, retarding of post prandial clearance of lipids contributes to hyperlipidemia. Cardiac sympathetic activation is a probable cause of sudden death in hearth failure. A trophic effect of sympathetic activation on cardiovascular growth is also likely, contributing to the development of left ventricular hypertrophy. Consequently, one of the major aims of antihypertensive therapy should be to attenuate sympathetic tone. It is possible that, among the antihypertensive drugs available, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk.

Herbal medicines as diuretics: A review of the scientific evidence

“…Indeed, ACE inhibitors work by interrupting the conversion of angiotensin-I to angiotensin-II and therefore attenuating the arterial constrictor effects of angiotensin-II (Wright et al, 2005). Beta receptor blockers act to counter the stimulatory effects of vascular and cardiac noradrenergic receptors (Rabbia et al, 2001). CCB's inhibit calcium entry thus decreasing the tone of vascular smooth muscle and promoting vasodilatation (Godfraind, 2006).…”

Contrasting Metabolic Effects of Antihypertensive Agents

“…Human studies are not unanimous, but in general thiazide diuretics and ␤-adrenergic antagonists have slight adverse effects, calcium channel blockers are mixed, and ␣ 1 -antagonists and inhibitors of the reninangiotensin system have positive effects (Rabbia et al, 2001;Imazu, 2002). Several theories have been advanced to account for the metabolic effects of various classes of antihypertensives.…”

Effects of Antihypertensive Drugs on the Renin-Angiotensin System in Essential Hypertension

“…The imidazoline (I1)-agonists also cause peripheral sympathetic inhibition, triggered at the level of central nervous imidazoline receptors, which are predominant in the anterior ventro-lateral medulla. [20] Although the principal actions of clonidine are linked to its centrally mediated suppression of sympathetic activity, the inhibition of the renin axis may also contribute to its antihypertensive effect. Although the quantitative importance of this latter action is not clear, it can be observed an initial suppression of the vasoconstriction mediated by the reninangiotensin system, followed by a long-term antihypertensive action due to the suppression of aldosterone.…”

“…[15] By blocking sympathetic influence on vascular smooth muscle, these agents act as both arterial and venous vasodilators. [20] Peripheral resistance falls without major changes in cardiac output, partly because of a balance between a decrease in venous return (preload) and a modest reflex sympathetic stimulation (consequence of vasodilatation). [15] The a 1 -adrenergic blockers have little or no clinical effect on glomerular filtration rate and renal blood flow [21] even if renal vascular resistance is reduced.…”

“…This effect may be attributable to the reflex activation of sympathetic nervous system and or renin secretion. [20] 1.3 a 1 -Adrenoceptor Antagonists (a 1 -Blockers) a 1 -Adrenoceptors are located post-synaptically and mediate vasoconstriction through endogenously released norepinephrine. [5] Until 1987, prazosin was the only selective a-blocker available, but other agents are now available.…”