Previous reports (1-9) have delegated a secondary role to anterior pituitary hormones in the control of aldosterone secretion.' Although hypophysectomy resulted in decreased aldosterone secretion (3) or reduced urinary aldosterone output (2), hyperaldosteronuria, marked sodium (Na) retention and ascites occurred in the absence of the adenohypophysis in dogs with thoracic inferior vena cava constriction (2). Also, in patients with hypopituitarism, Luetscher and Axelrad (6) and Hernando and associates (7) found that urinary aldosterone output was within normal limits in some patients on an unselected diet or a normal salt intake, and Liddle, Duncan 'and Bartter (8) reported hyperaldosteronuria in one patient with hypopituitarism on a low Na diet.However, no conclusive evidence of hypersecretion 1 of aldosterone in the absence of anterior pituitary hormones has been reported. The critical pertinent data on the rate of aldosterone secretion during stimulation which produces hypersecretion in normal animals have not been reported for hypophysectomized dogs or patients. It is important that studies in man be conducted on hypophysectomized patients since patients with so-called panhypopituitarism may not have loss of all anterior pituitary function. Furthermore, our knowledge is incomplete on the importance of specific anterior pituitary hormones. Several studies (3,7,(8)(9)(10) have demonstrated an increase in aldosterone secretion or urinary aldo-* This investigation was aided in part by Grant A-1944 from the National Institutes of Health, Bethesda, Md.1 The phrases "aldosterone secretion" or "hypersecretion of aldosterone" have been used to refer to actual measurements of the rate of secretion by the adrenal gland into the effluent plasma and are to be distinguished from urinary aldosterone excretion. sterone excretion following administration of various corticotropin preparations, but the data are inadequate to establish the role of ACTH in secondary hyperaldosteronism.2The question of the role of the anterior pituitary in the control of aldosterone secretion was reopened by the finding of a 76 to 97 per cent fall in adrenal vein aldosterone output following hypophysectomy of dogs with experimental secondary hyperaldosteronism ( 11). In the present report, data are presented on the efficacy of ACTH 3 in preventing this fall in aldosterone secretion which follows hypophysectomy. Large doses of cortisone have been administered to inhibit ACTH secretion in dogs with hyperaldosteronism secondary to caval constriction; the resultant effects on aldosterone and corticosterone production were observed. Subsequently, the effects of hypophysectomy and ACTH were studied in these animals. Also, the effects of synthetic a-melanophore-stimulating hormone (MSH) and of highly purified preparations of natural a-and ,B-MSH have been studied. Attempts have been made to stimulate hypersecretion of aldosterone in simple hypophysectomized dogs by 1) a low Na diet and 2) acute constriction of the thoracic inferior vena cava.2 In this pap...