Kono T, Ikeda F, Oseko F, Ohmori Y, Nakano R, Muranaka H, Taniguchi A, Imura H, Khosla M C, Bumpus F M
Acta Endocrinol (Copenh). 1982 Apr;99(4):577-84. doi: 10.1530/acta.0.0990577.
The biological activity of des-asp1-des-arg2-angiotensin II (3-8AII) was studied in man. When 3-8AII was infused iv at rates of 22 and 308 pmol (17.5 and 250 ng)/kg . min separately into 5 normal men each for 120 min, blood pressure showed no change, plasma renin activity (PRA) decreased gradually and plasma aldosterone showed a gradual slight increase. The lower dose of 3-8AII partially inhibited captopril-induced PRA increase and plasma aldosterone decrease in the same 5 normal men and the higher dose of the hexapeptide completely abolished them. In one of the 5 normal men blood pressure rose in response to doses of 3-8AII greater than 2220 pmol (1750 ng)/kg . min. When 3-8AII was infused iv at 308 pmol/kg . min into 2 patients with Bartter's syndrome for 60 min, it caused marked decrease in PRA and plasma aldosterone but no change in blood pressure. This decrease in plasma aldosterone is thought to be secondary to the decrease in PRA. From these results it is evident that 3-8AII has a minimal pressor action, a weak aldosterone-stimulating action and a significant renin-suppressing action in man and this PRA-lowering action is thought to be due to direct inhibition of renin release by its whole molecule or a smaller part of the molecule.
