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Second Division, Department of Internal Medicine, Kyoto University School of Medicine Shogoin, Sakyo-ku, Kyoto 606, Japan
College of Medical Technology, Kyoto University Shogoin, Sakyo-ku, Kyoto 606, Japan
Address requests for reprints to: Tsuyoshi Kono, M.D., Second Division, Department of Internal Medicine, Kyoto University School of Medicine, Shogoin, Sakyo-ku, Kyoyo 606, Japan.
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 [angiotensin 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 reninangiotensin-aldosterone system.
* This work was supported by Grant 457598 from the Ministry of Education in Japan.
Received February 12, 1979.
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