THE REGULATION OF ALDOSTERONE PRODUCTION IN NORMAL AND SODIUM-DEFICIENT RATS

Abstract

SUMMARY Aldosterone secretion of rats on a standard diet, as determined by the rate of aldosterone produced by adrenal tissue in vitro, was not affected by exposure to ether, by hypophysectomy or by nephrectomy. Administration of high doses of long-acting corticotrophin (ACTH; 1·5 units) to rats hypophysectomized 24 hr. previously also failed to affect the rate of aldosterone production in vitro in rats on the standard diet. Only hypophysectomy and nephrectomy in the same rat induced a significant decrease in aldosterone production in vitro 6 hr. after operation in rats fed the standard diet. Aldosterone production in vitro increased in rats fed a sodium-deficient diet. The increment was more pronounced in rats maintained on the diet for 14- than for 10-days. Hypophysectomy, or nephrectomy, caused no decrease in aldosterone production, when compared to sham-operated rats. However, hypophysectomy and nephrectomy together caused a marked decline in the rate of aldosterone production in vitro 6 hr. after operation as compared with sham-operated or non-operated rats. The administration of relatively small amounts of ACTH (8 m-u.) induced a marked increase in the rate of aldosterone production in vitro of intact, and hypophysectomized sodium-deficient rats. The results indicate that in the rat, as in other species, both the kidney and the pituitary contribute to the maintenance of the basal rate of aldosterone production in animals in normal sodium-balance and that these organs are responsible for the increased rate of aldosterone production in dietary sodium restriction. ACTH, however, though a potent stimulus for aldosterone secretion, appears only to augment the already enhanced production of aldosterone in the sodium-deprived rat.