Circulation, Vol 75, 1030-1036, Copyright © 1987 by American Heart Association
RE Schmieder, FH Messerli, GE Garavaglia and BD Nunez
The cardiovascular effects of intravenous verapamil and 3 months of oral
administration of a slow-release form of verapamil (verapamil-SR) were
studied in 10 patients with mild-to-moderate essential hypertension.
Intravenous verapamil reduced arterial pressure by 15% (p less than .01)
through a fall in total peripheral resistance of 29% (p less than .01);
provoked a reflexive rise in heart rate (by 19%, p less than .02), cardiac
output (by 74%, p less than .01), and plasma catecholamines; and shifted
intravascular volume toward the cardiopulmonary circulation indicating
peripheral venoconstriction. Quite in contrast to the immediate effects of
the intravenous drug, oral therapy with verapamil-SR for 2 to 3 months
lowered arterial pressure effectively (by 15%, p less than .01) by inducing
vasodilation of 15% (p less than .02), but without causing reflex
tachycardia, activation of the sympathetic-adrenergic or renin-angiotensin
systems, or volume expansion. Oral therapy with verapamil-SR preserved
systemic and renal blood flow and slightly reduced cardiac mass (by 6%, p
less than .05) and renal vascular resistance (by 25%, p less than .05).
Whereas intravenous verapamil tended to depress myocardial contractility,
oral verapamil-SR did not at all affect myocardial contractility or left
ventricular function. These cardiovascular effects make verapamil-SR an
excellent agent for long-term antihypertensive therapy.
ARTICLES
Cardiovascular effects of verapamil in patients with essential hypertension
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