Effect of Sodium Depletion on the Steroidogenic and Pressor Actions of Angiotensin in the Rat

Abstract

To investigate the relative roles of angiotensin [A] II and des-Asp1-AII (AIII) in the control of blood pressure and aldosterone [ALDO] release, the effects of 7 A agonists on mean arterial blood pressure and serum ALDO concentrations were compared in normal and Na-depleted, conscious rats. In normal rats, AI, .alpha.-Asp1-AII, .beta.-Asp1-AII, and AII-amide were equipotent in elevating mean arterial blood pressure. AIII, des-Asp--AI and poly-O-acetylserine-AII were 25, 25 and 41% as potent as AII, respectively. After Na depletion, pressor responses to these A peptides were reduced approximately 60-80% when compared with control responses. In contrast, pressor responses to noradrenaline [norepinephrine] were not significantly affected by Na depletion. AII, .beta.-Asp1-AII, AII-amide and AIII were equipotent in increasing serum ALDO concentrations in normal animals. AI was 59% and des-Asp1-AI only 5% as potent as AII in their abilities to release ALDO. After Na depletion, control serum ALDO concentrations increased as did the slope of the dose-response curve for each A peptide. AII was the most potent steroidogenic peptide in Na-depleted rats with AIII and .beta.-Asp1-II being 27%, AI 7%, AII-amide 3%, and des-Asp1-AI 1% as potent as AII in releasing aldosterone. Poly-O-acetyl-serine-AII has less steroidogenic effect than AII or AIII in both normal and Na-depleted animals. Infusions of the AII antagonist, Sar1-Ile8-AII, and the AIII antagonist, Ile7-AIII, enhanced ALDO release in normal rats without altering blood pressure. After Na depletion, Sar1-Ile8-AII decreased blood pressure without affecting ALDO release whereas Ile7-AIII diminished ALDO release without altering blood pressure. AII, independent of its conversion into AIII, appears to be an important regulator of steroidogenesis in the rat in normal Na states. In Na depletion, the octapeptide retains significant steroidogenic activity; however, the contribution of AIII to its steroidogenic effects is increased.