Hemodynamic effects of the converting enzyme inhibitor teprotide in normal- and high-renin hypertension.
The hemodynamic effects of the converting enzyme inhibitor teprotide (SQ 20881) were investigated in five patients with normal plasma renin activity who were normotensive during the study (group I), in five patients with hypertension and normal plasma renin activity (group II), and in five patients with hypertension and high plasma renin activity (group III). No significant hemodynamic changes were observed during teprotide administration in group I. In group II there was a decrease in mean arterial pressure by 10 +/- 2% (p < 0.005) that was associated with a decrease by 16 +/- 7% (p < 0.05) in stroke volume and cardiac output, possibly due to venodilatation and without a concurrent change in total peripheral resistance. In group III the larger decrease of 19 +/- 4% (p < 0.005) in mean arterial pressure was due to a decrease by 30 +/- 3% (p < 0.005) in peripheral resistance. In this group stroke volume and cardiac output increased by 13 +/- 2% (p < 0.025). There were no compensatory changes in heart rate despite the decrease in mean arterial pressure and vasodilatation. These results indicate that teprotide decreases arterial pressure by a dual hemodynamic mechanism. Cardiac output is increased by teprotide in patients with high-renin hypertension who exhibit the greatest decrements in peripheral resistance.
D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors; D001920:Bradykinin / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009842:Oligopeptides / Q000494:pharmacology*; D012083:Renin / Q000097:blood*; D013722:Teprotide / Q000494:pharmacology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D009842:Oligopeptides; D013722:Teprotide; D012083:Renin; D001920:Bradykinin