Circulation, Vol 57, 373-378, Copyright © 1978 by American Heart Association
JG de Carvalho, FG Dunn, DC Kem, SG Chrysant and ED Froholich
Angiotensin antagonists have proved useful in elucidating the clinical role
of the renin-angiotensin system; and their diagnostic and therapeutic
efficacy in hypertension has been the subject of many reports but the
hemodynamic effects remain unknown. Therefore, saralasin was infused
intravenously (1.3 mg/min for 30 min) in 26 sodium-depleted patients with
hypertension. Systemic hemodynamic alterations were determined before,
during, and after infusion. On the basis of mean arterial pressure (MAP)
changes, patients were classified as responders, nonresponders, or
pressorresponders (MAP changes greater than or equal to 10 mm Hg). MAP fall
in responders was achieved through reduced cardiac output and/or total
peripheral resistance, with minimal or absent reflexive heart rate
increase. In nonresponders, despite no change in MAP, output fell in
parallel with stroke index and left ventricular ejection rate, In
pressorresponders, saralasin increased vascular resistance. Thus, in
addition to variable effects on vascular receptors, saralasin produced
inhibitory cardiac effects either through altered venous return or
inhibition of contractility.
ARTICLES
Hemodynamic correlates of saralasin-induced arterial pressure changes
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