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Recent studies (1-5) indicate that the immediate stimulus to aldosterone production is humoral. Evidence for secretion of an aldosterone-stimulating hormone (ASH) by the kidney in response to acute blood loss was presented at the Laurentian Hormone Conference in 1960 (4). The present study is concerned with the locus of secretion of an ASH in two other experimental situations: 1) hyperaldosteronism secondary to chronic constriction of the thoracic inferior vena cava, and 2) chronic Na depletion. The present data provide evidence for extension of our knowledge of an ASH to clinical states with edema; the dog with thoracic caval constriction is very similar in regard to electrolyte and water metabolism and hyperaldosteronism to the patient with cirrhosis of the liver and ascites. Studies of the origin of secretion of an ASH during Na depletion were made because changes in electrolyte intake constitute one of the most important physiological mechanisms in the regulation of aldosterone secretion. Evidence for secretion of an ASHby the kidney in these two experimental situations was obtained by study of the effects of acute nephrectomy on aldosterone secretion.

RENAL ORIGIN OF AN ALDOSTERONE-STIMULATING HORMONE IN DOGS WITH THORACIC CAVAL CONSTRICTION AND IN SODIUM-DEPLETED DOGS