Long-term clonidine effects on autonomic function in essential hypertensive man.

Abstract:

:Acute studies of clonidine suggest that it lowers blood pressure by central enhancement of baroreflex sensitivity coupled with diminished evidence of sympathetic outflow, but longterm clonidine data have not been conclusive. We examined effects of one month of low dose clonidine (0.4 +/- 0.15 mg/day) alone in 13 essential hypertensive men, assessing several biochemical indices of sympathetic function, as well as physiologic parameters, including baroreflex sensitivity, the cold pressor test, and the hypotensive response to alpha adrenergic blockade. Clonidine diminished mean arterial pressure (from 104 +/- 5 to 84 +/- 3 mmHg; p less than 0.01), without associated changes in several biochemical parameters of sympathetic outflow (urinary excretion of catecholamines, metanephrines, and vanillylmandelic acid; all p greater than 0.1). Circulatory baroreflex function was not enhanced by clonidine, during either the amylnitrite test or the phenylephrine test, before or after parasympathetic blockade with atropine. The cold pressor test, an index of efferent sympathetic pressor function, was also unaltered. The enhanced mean arterial pressure response to phentolamine during clonidine therapy (from a fall of 14.8 +/- 4.3 to 39.4 +/- 5.2 mmHg, p less than 0.01), suggested an increase in alpha adrenergic vascular tone, perhaps mediated by clonidine's alpha agonist properties in vascular smooth muscle. The antihypertensive mechanism of longterm low dose clonidine cannot reliably be ascribed either to baroreflex enhancement or to suppression of sympathetic outflow.

journal_name

Eur J Clin Pharmacol

authors

Cohen IM,O'Connor DT,Preston RA,Stone RA

doi

10.1007/BF00558378

subject

Has Abstract

pub_date

1981-01-01 00:00:00

pages

25-32

issue

1

eissn

0031-6970

issn

1432-1041

journal_volume

19

pub_type

临床试验,杂志文章,随机对照试验
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