Intracerebroventricular infusion of angiotensin II inhibits aldosterone secretion

The role of angiotensin II (AII) in the control of aldosterone secretion by action on the central nervous system (CNS) was studied using anesthetized, sodium-deprived dogs. Changes in plasma levels of sodium and potassium were measured, and changes in plasma concentration of cortisol and plasma renin activity (PRA) were used as indices of changes in ACTH secretion and in plasma levels of AII. Infusion of AII (6 ng/min) into the lateral cerebral ventricle decreased aldosterone levels and reduced PRA and plasma potassium concentration. Because there were no changes in plasma sodium or cortisol levels, the decrease in aldosterone secretion may have been secondary to decreased plasma AII or potassium concentration. In view of the uncertain physiological role of endogenous AII in the brain, blockers of the renin-angiotensin system were also infused. Central blockade of AII produced by administration of the converting enzyme inhibitor, SQ 20881 (0.5-15 μg/min), increased plasma aldosterone concentration but had no effect on PRA and sodium or potassium concentrations. These results suggest that endogenous angiotensin acts on the brain to inhibit aldosterone secretion. This conclusion was substantiated by the finding that intraventricular infusion of the competitive inhibitor [Sar¹,Ala⁸]-AII (P-113) also increased plasma aldosterone levels. The rise in aldosterone concentration occurred independently of concomitant changes in PRA (plasma AII levels), plasma electrolyte concentration, and plasma cortisol concentration (ACTH). These data support the hypothesis that an as yet unidentified factor may be involved in the control of aldosterone secretion.