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PubMed1976

[Sympatholytics].

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Adrenergic alpha-Agonists↗
PubMed1993

[Effect of three antihypertensive drug groups on lipid metabolism. Effects of alpha receptor blockers, central sympatholytic drugs and vasodilators].

Basic remarks and aims: Alpha-receptor blockers, central sympathicolytic agents and vasodilators are all drugs that are often used to treat hypertension. On the basis of a study of the literature, the effects of these groups of substances on lipid metabolism are described. Main points discussed: Although the data available are few, vasodilators, in particular dihydralazine and hydralazine appear to have no unfavorable effect on serum lipids. Nor do the centrally acting alpha-receptor agonists, such as methyldopa and clonidine have any unfavorable effect, with the exception of the decrease in the HDL cholesterol observed under methyldopa. The selective alpha-1-receptor blockers, prazosin, doxazosin and urapidil, even have a positive effect of varying degree on lipid metabolism: increase in HDL cholesterol and decrease in triglycerides. Long-term studies over a number of years are, however, lacking. The effect of labetalol, reserpine and guanethidine on lipid metabolism cannot yet be definitively assessed owing to a lack of data.

Adrenergic alpha-Antagonists↗
PubMed1994

Ketanserin's sympatholytic and serotonin2-receptor blocking actions precede the hypotensive effects.

The hypotensive action of ketanserin in humans remains incompletely defined but may be mediated by factors unrelated to vascular alpha 1 or serotonin2-receptor blockade. We examined the effects of ketanserin on indices of sympathetic drive, alpha 1- and serotonin2-receptor responses, and sympathetic tone in 13 elderly men with mild hypertension. Studies were performed after ten days and six weeks of double-blind assignment to placebo and ketanserin 40 mg twice daily. An eight week long single-blind, placebo washout period separated the double-blind phases. In the entire group, ketanserin lowered BP and heart rate significantly after six weeks but not at ten days. In contrast, plasma noradrenaline, an index of sympathetic drive, and platelet aggregation in response to 1 microM serotonin, an index of serotonin2-receptor antagonism, declined significantly after both ten days and six weeks (P < 0.05) on ketanserin versus placebo. Mean BP after six weeks on ketanserin fell to > 10% in seven patients (responders) and to < 10% in six subjects (nonresponders). Responders had higher baseline SBPs and heart rates compared with nonresponders. Even in responders, BP was reduced at six weeks but not after ten days on ketanserin versus placebo. Plasma and platelet noradrenaline, plasma renin activity, and platelet responses to serotonin at baseline and during ketanserin did not distinguish between responders and nonresponders. Ketanserin reduces sympathetic drive and antagonizes serotonin2-receptors in the short term. The relationship of these actions to the hypotensive effect of ketanserin, which is delayed and dependent on the initial BP, is unclear.

Double-Blind Method↗