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Previous studies (2-4) have demonstrated that nephrectomy lowers control aldosterone secretion rates and prevents the increase in aldosterone secretion that follows hemorrhage. Injection of saline extracts of kidneys (3, 4) from normal dogs into hypophysectomized, nephrectomized dogs stimulated aldosterone secretion markedly while also stimulating 17-hydroxycorticoid and corticosterone secretion. A marked pressor response also occurred. These observations suggested that the kidney secreted an aldosterone-stimulating factor. The stimulation of glucocorticoid secretion by the saline kidney extracts raised the possibility that ACTH was present in the kidney extract. This possibility appeared to be supported by the finding of Richards and Sayers (5) that exogenous ACTH accumulated preferentially in the kidney. On the other hand, the pressor response produced by the saline kidney extracts suggested that the extracts contained renin. Considerable indirect evidence (6) suggested that the reninangiotensin system may play an important role in the regulation of aldosterone secretion. To investigate the nature of this kidney factor, the effect of several substances on adrenocortical secretion of hypophysectomized, nephrectomized dogs has been studied. Saline extracts of kidneys from hypophysectomized dogs, and dog anterior pituitaries, commercial ACTH, semipurified renin extracts, and synthetic angiotensin II have been assayed. The results indicate that the aldosteronestimulating factor in the dog kidney is renin.

THE NATURE OF THE ALDOSTERONE-STIMULATING FACTOR IN DOG KIDNEYS*