THE ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN THE CONTROL OF ALDOSTERONE SECRETION*

Abstract

Within the last year, evidence (1-4) has ac- cumulated to show that the kidney secretes a hor- mone which is a prime regulator of aldosterone secretion. The renal origin of an aldosteronestimulating hormone (ASH) has been demon- strated following acute blood loss (1-3), during chronic thoracic caval constriction (4), and dur- ing chronic Na depletion (4). Nephrectomizedhypophysectomized dogs failed to respond to acute hemorrhage with an increase in aldosterone secretion, and acute bilateral nephrectomy of hypophysectomized caval and hypophysectomized Na- depleted dogs resulted in a marked drop in aldosterone secretion. Furthermore, crude saline extracts of kidney produced a striking increase in aldosterone secretion (1-5). In malignant ex- perimental renal hypertension, hyperaldosteronism was consistently present (6). These findings and the reports that renin preparations (6) and syn- thetic angiotensin II (6-8) increase the rate of aldosterone production suggest the possibility that ASH is renin.