Abstract

There is evidence suggesting that the control of aldosterone secretion is relatively independent of the pituitary gland. This is based on morphological studies in the rat (1), on indirect assessments of adrenal secretion during metabolic studies in man (2), and on direct estimations of adrenal hormone secretion in the rat (3, 4) and dog (5-7). The morphological studies of Deane and Masson (8), which indicate that renin may stimulate the adrenal cortex in the rat, the results of Genest and his colleagues (9), which suggest that arterial hypertension may be associated with an increased excretion of aldosterone in man, and the demonstration by Genest ( 10, 11 ) and Laragh (12) and their colleagues that angiotensin II stimulates excretion (10, 11) and secretion (12, 13) of aldosterone suggest that the kidney may have some influence on the rate of secretion of adrenal hormones. Recently, Pronove, MacCardle, and Bartter (14) described a dwarfed, normotensive child who was suffering from the effects of excessive production of aldosterone. This was associated with a remarkable hypertrophy and hyperplasia of the juxtaglomerular apparatus in the kidney. The syndrome has been found subsequently in two other patients with hyperaldosteronism (15, 16). The observations suggested that the kidney itself was in some way responsible for the overproduction of aldosterone. The present experiments, performed in the dog, were designed to test the hypothesis that the normal kidney contains material capable of stimulating the adrenal cortex. This was found to be so (17, 18), in agreement with results simultaneously obtained by Mulrow, Ganong, Cera, and Kuljian (19) and by Davis and associates (20, 21). Accordingly, further studies were designed to see whether the pattern of response of the three important adrenocortical steroid hormones (aldosterone, cortisol, and corticosterone) was such as to suggest that this renal stimulus is involved in the mediation of aldosterone secretion physiologically.

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