RELATION OF RENIN, ANGIOTENSIN II, AND EXPERIMENTAL RENAL HYPERTENSION TO ALDOSTERONE SECRETION*

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Abstract
Infusion of renin into hypophysectomized nephrectomized dogs increased the rates of secretion of aldosterone, corticosterone and Porter-Silber chromogens by a non-ACTH mechanism. Infusion of synthetic angiotensin II into hypophysectomized-nephrectomized or simple-hypophysectomized dogs (only anterior pituitary removed) likewise augmented the production of each of the steriods measured; a decrease in the rate of infusion of angiotensin II reduced in the increment in corticosterone secretion to a far greater extent than the increment in aldosterone secretion. With doses of angiotensin II too small to elicit a blood pressure response, physiologically significant increases in aldosterone secretion were sometimes observed. At this very low dosage level, the increments in cortisterone output were quantitatively slightly greater than those of aldosterone but were at a level which usually has no physiological effect, and no significant changes in Porter-Silber chromogen production occurred. The renin content of the kidneys of dogs with benign renal hypertension was only slightly increased, and aldosterone secretion was within normal limits in these animals. A 10-fold increase in the renin content of the kidneys was observed in dogs with malignant renal hypertension, and aldosterone output was markedly increased, by a non-ACTH mechanism, in this group of dogs. These data are consistent with the concept that the renin-angiotensin II system plays an important physiological role in the regulation of aldosterone secretion.