Hypertension, Vol 2, 700-707, Copyright © 1980 by American Heart Association
G Mancia, A Ferrari, L Gregorini, MC Ferrari, C Bianchini, L Terzoli, G Leonetti and A Zanchettie
Prazosin, an antihypertensive agent that reduces blood pressure (BP) mainly
through a blockade of alpha-adrenergic receptors, may, in theory, affect
sympathetic control of circulation to an extent that impairs circulatory
hemeostasis. This possibility was studied in subjects with essential
hypertension by examining the cardiovascular effects of several stimuli
that induce a powerful and diversified activation of the sympathetic
noradrenergic activity (dynamic and isometric exercise, cold exposure) and
of stimuli that exert a powerful inhibitory influence upon the sympathetic
nervous system (carotid baroreceptor reflex). Before and after 15 days of
continuous administration of prazosin (2-5 mg), 3 times a day, measurements
were made of BP (intraarterial catheter), heart rate, cardiac output
(thermodilution), and peripheral resistance. Prazosin reduced mean arterial
pressure (10%) and peripheral resistance (9%) at rest, and it did not
affect heart rate and cardiac output. Neurally mediated changes in arterial
pressure, cardiac output, and peripheral resistance during dynamic or
isometric exercise and cold exposure were unaffected by the drug; also
unaffected were the cardiovascular responses to increase and decrease in
carotid baroreceptor activity obtained by varying carotid transmural
pressure through a variable neck pressure chamber device. Thus, the
hypotensive and vasodilating effect of prazosin in essential hypertension
is not accompanied by an impaired response to neural excitation influences
upon the cardiovascular system. Also, the inhibitory influences originating
from the carotid baroreflex are unchanged. These data indicate that
circulatory homeostasis is largely preserved during administration of
prazosin at clinically effective doses.
ARTICLES
Effects of prazosin on autonomic control of circulation in essential hypertension
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