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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.
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SUMMARY
Hypophysectomy abolishes the aldosterone secretory response to sodium deficiency in rats. Sodium deficiency causes a significant increase in plasma renin activity in chronically hypophysectomized rats which is of the same order as that found in intact animals.
Long-term treatment with either adrenal maintenance doses of corticotrophin (ACTH) or with growth hormone (STH) did not affect the low rate of aldosterone production of hypophysectomized rats on a sodium-deficient diet. However, ACTH and STH given simultaneously restored the aldosterone secretory response to sodium deficiency in chronically hypophysectomized rats.
The plasma renin activity of hypophysectomized rats on a sodium-deficient or a normal diet remained unaltered during treatment with either ACTH or STH or with the two hormones given simultaneously. This was also reflected in the systolic blood pressure of rats which, under the conditions used, did not change when the animals were sodium-deficient, or after hypophysectomy or hormone treatment.
These results indicate that the effect of STH, in restoring the aldosterone secretory response to sodium deficiency in the presence of adrenal maintenance doses of ACTH in chronically hypophysectomized rats, is independent of changes in the renin-angiotensin system.
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SUMMARY
Daily administration of growth hormone (STH) to hypophysectomized rats treated with adrenal maintenance doses of corticotrophin restored the aldosterone secretory response (as measured by the synthetic capacity of the adrenal in vitro) to sodium restriction. Treatment with STH for the first 2 days after hypophysectomy or on the 7th day after hypophysectomy failed, but treatment during the 6th and 7th day after hypophysectomy with 100, 200 or 400 μg STH/day restored the aldosterone secretory response to sodium deprivation in a dose-dependent manner.
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SUMMARY
Studies of the rate of aldosterone production in vitro of adrenals of rats hypophysectomized before dietary sodium restriction showed that hypophysectomy not only prevented the increases in aldosterone production observed in intact, Na-deprived rats, but also depressed the level of aldosterone production to below that of intact rats maintained on a normal diet. Rats hypophysectomized for a similar period of time but maintained on the normal diet showed a similar decrease.
Experiments on adeno- and neuro-hypophysectomized rats indicated that the pituitary factor required for the normal mineralocorticoid response to dietary sodium restriction resides in the anterior pituitary.
Treatment of hypophysectomized rats during dietary sodium restriction with doses of a long-acting corticotrophin (ACTH) prevented adrenal atrophy and maintained a normal glucocorticoid response to intravenous injections of ACTH, but failed to increase aldosterone production rates in vitro to levels above that of intact rats on a normal diet; it also failed to restore the enhanced adrenocortical sensitivity to the stimulating effect of aldosterone production of intravenously injected ACTH which is characteristic of acutely hypophysectomized, Na-deficient rats. Treatment with anterior pituitary powder (8–12 mg./day) for similar periods, however, restored the aldosterone production of adrenals in vitro of hypophysectomized, Na-deprived rats to levels nearly indistinguishable from those of acutely hypophysectomized, Na-deprived controls. The same doses of anterior pituitary powder were shown not to have any demonstrable effect on the aldosterone production of adrenals in vitro of intact rats on a normal diet.
These results are interpreted as indicating the existence of a pituitary factor other than ACTH which stimulates aldosterone secretion. This factor does not appear to act directly on the adrenal cortex or to stimulate the secretion of specific glomerulotropic substances, but probably exerts its effect by maintaining the normal functional capacity of some as yet undefined tissues which secrete glomerulotropic substances in response to dietary sodium restriction.
