In the dog, the renin--angiotensin system appears to be a primary control mechanism for aldosterone secretion since angiotensin II blockade decreased aldosterone production to undetectable levels. Angiotensin II blockade also decreased cortisol secretion strikingly in dogs with thoracic caval constriction, a finding which suggests the presence of an angiotensin II receptor in the two inner zones of adrenal cortex. An important incidental finding after angiotensin II blockade in both sodium-depleted dogs and dogs with thoracic caval constriction was the striking drop in arterial pressure. It is suggested that angiotensin II acts on the peripheral arterioles to provide an important compensatory mechanism and, thereby, maintain arterial pressure in these low cardiac output states. In the rat, both the nonapeptide converting enzyme inhibitor and [Sar1, Ala8]-angiotensin II produced a marked decrease in aldosterone secretion in hypophysectomized, sodium-depleted animals. Both synthetic angiotensin II and its heptapeptide fragment produced striking increases in aldosterone secretion when the obscuring effect of ACTH was excluded in the rat. These findings provide evidence that the renin--angiotensin system is an important control mechanism for aldosterone biosynthesis in the rat.