No substrate specificity of converting enzyme for N-terminal substituted angiotensin I in man.
In 5 normal men sarcosine1-angiotensin II (Sar1-ANG II) (Exp. 1) and sarcosine1-angiotensin I (Sar1-ANG I) (Exp. 2) infused iv at a rate of 5 pmol/kg X min from 0900 h to 0930 h caused the same degree of rise in blood pressure (BP). But 100 mg of captopril given orally at 0800 h (Exp. 3) completely abolished the BP rise by Sar1-ANG I. In Exps. 1 and 2 plasma renin activity (PRA) decreased and plasma aldosterone (PA) increased after the infusions. In Exp. 3 PRA increased markedly and PA decreased 60 min after captopril, and at 30 min of Sar1-ANG I infusion PRA decreased to the pre-captopril level despite no BP change but PA was kept at the pre-infusion level. Hence, substrate specificity of converting enzyme previously demonstrated for N-terminal deleted ANG I was not shown for N-terminal substituted ANG I in man because the conversion of Sar1-ANG I to Sar1-ANG II was 100%. Sar1-ANG I may possibly inhibit renin release in normal men.
D000328:Adult; D000803:Angiotensin I / Q000031:analogs & derivatives* / Q000494:pharmacology; D000804:Angiotensin II / Q000031:analogs & derivatives / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D006801:Humans; D008297:Male; D013379:Substrate Specificity
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; C032651:angiotensin II, Sar(1)-Ile(5)-; C051901:angiotensin I, Sar(1)-; D000803:Angiotensin I; D002216:Captopril