No Substrate Specificity of Converting Enzyme for N-Terminal Substituted Angiotensin I in Man

Abstract

In 5 normal men sarcosinel-angiotensin II (Sarl-ANG II) (Exp. 1) and sarcosinel-angiotensin I (Sarl-ANG I) (Exp. 2) infused iv at a rate of 5 pmol/kg-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 Sarl-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 Sarl-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.

Key Words:

• angiotensin-converting enzyme
• ACE
• substrate specificity ACE inhibitor
• captopril
• N-terminal substituted angiotensin I
• sarcosinel-angiotensin I
• sarcosinel-angiotensin II
• pressor action
• renin-suppressing action
• steroidogenic action
• aldosterone-stimulating action in normal men