Role of renin-angiotensin and kallikrein-kinin systems on the mechanism of the hypotensive effects of converting enzyme inhibitor, alacepril.
In four patients with essential hypertension and one patient with renovascular hypertension, decreases in blood pressure and plasma angiotensin II levels, and increases in plasma renin activity and plasma kinin levels were observed during eight days of alacepril treatment. Significant correlations between the changes in mean arterial pressure and those in plasma angiotensin II or kinin levels were observed positively or negatively, respectively, in the essential hypertensives. These findings suggest that the hypotensive effect of alacepril might be caused mainly by a decrease in plasma angiotensin II levels and, at least in part, by an increase in plasma kinin levels.
D000328:Adult; D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000031:analogs & derivatives* / Q000494:pharmacology; D005260:Female; D006801:Humans; D006977:Hypertension, Renal / Q000503:physiopathology; D007610:Kallikreins / Q000502:physiology*; D007705:Kinins / Q000097:blood / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D007705:Kinins; D000804:Angiotensin II; D002216:Captopril; D007610:Kallikreins; C046835:alacepril