Kono T, Ikeda F, Oseko F, Imura H, Endo J
J Clin Endocrinol Metab. 1980 Jan;50(1):40-5. doi: 10.1210/jcem-50-1-40.
The biological activity of des-Asp1-angiotensin I (des-Asp1-AI) was studied in five normal men. An iv infusion of 300 ng (258 pmol)/kg.min des-Asp1-AI caused a remarkable rise in blood pressure, a decrease in PRA, and an increase in plasma aldosterone concentration. The pressor and steroidogenic actions of this dose of des-Asp1-AI were slightly less than those of 100 ng (111 pmol)/kg.min des-Asp1-angiotensin II [Angotensin III (AIII)] which we reported previously and were abolished by a single oral administration of 100 mg of a converting enzyme inhibitor, SQ 14225. These results indicate that in man, as in animals, a rise in blood pressure and an increase in plasma aldosterone concentration after an infusion of des-Asp1-AI are entirely due to the actions of AIII converted from this nonapeptide, and that the conversion rate of des-Asp1-AI to AIII in normal men is less than 43%. This is much less than the conversion rate of angiotensin I to angiotensin II. It seems unlikely that des-Asp1-AI has physiological significance in the human renin-angiotensin-aldosterone system.
