Hemodynamic correlates of saralasin-induced arterial pressure changes.
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.
D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000031:analogs & derivatives*; D001794:Blood Pressure / Q000187:drug effects*; D002302:Cardiac Output / Q000187:drug effects; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D012504:Saralasin / Q000627:therapeutic use*; D014655:Vascular Resistance / Q000187:drug effects
D000804:Angiotensin II; D012504:Saralasin