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Male white rats were injected subcutaneously with graded doses of dexamethasone acetate 16 hr. before exposure to noxious stimuli. The rate of corticosteroid production by adrenal glands in vitro served as an index of ACTH release. The corticotrophic effect of environmental changes was readily suppressed by pretreatment with 50 μg. of dexamethasone, 125 μg. blocked the effect of histamine phosphate, 250 μg. the effect of noise and at least 500 μg. were needed to suppress the effect of unilateral adrenalectomy.
The adrenal response to ACTH was not affected by pretreatment with dexamethasone. The effect of lysine vasopressin on ACTH release diminished with increasing amounts of dexamethasone; a complete block was obtained with 500 μg.
In rats bearing extensive lesions in the median eminence pretreatment with dexamethasone also suppressed the corticotrophic effect of lysine vasopressin and of hypothalamic extracts. Dexamethasone pretreatment did not significantly alter the ACTH content of the pituitary of intact, shamoperated or lesioned rats. It is concluded that the blocking action of dexamethasone is located in the anterior pituitary.
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SUMMARY
The antidiuretic hormone (ADH) content of the hypothalamo-neurohypophysial system (HNS) and the excretion of AD-activity in the urine has been examined after pituitary stalk lesion in rats. In the oliguric phase which developed approximately 24 hr. after stalk destruction and lasted for about 3 days, the HNS was greatly depleted of ADH and the excretion of AD-activity in the urine was much above normal.
Implantation of posterior lobes obtained from intact adult rats under the kidney capsule of stalk-lesioned animals with a manifest diabetes insipidus produced oliguria similar to that found after stalk destruction. However, the antidiuretic effect of the implant lasted somewhat longer and the amount of AD-activity excreted in the urine was twice as high as that excreted in the oliguric period after stalk destruction.
Subcutaneous injection of lysine or arginine vasopressin in various vehicles into rats with manifest diabetes insipidus showed that the effect of these preparations on water intake and urine output was independent of the dosage used but seemed to depend on the rate of absorption from the subcutaneous tissue. The results indicate a relationship between duration of action and the amount of AD-activity excreted in the urine.
Hyperosmoticity induced by the subcutaneous injection of a 15% NaCl solution failed to release ADH irrespective of the hormone content of the HNS of stalk-lesioned rats.
In a number of stalk-lesioned rats the polyuria gradually disappeared several weeks after stalk destruction. The ADH content of the hypothalamus of these animals was nearly normal, but that of the posterior lobe was only about 10 % of that of intact controls. The urinary excretion of AD-activity in these animals was about half of that of the controls. In such rats ADH could be readily released from the HNS after loading with 15% NaCl, indicating that animals with a regression of the diabetes insipidus had resumed the production of ADH.
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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
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
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.
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Wisconsin Regional Primate Research Center, University of Wisconsin, Madison, Wisconsin 53706, U.S.A.
(Received 22 May 1978)
In a wide variety of species corticotrophin (ACTH) is known to stimulate the synthesis and secretion of adrenocortical steroids. Studies with rhesus monkeys have shown that these responses can be affected by a number of factors including the method of handling and the type of physical restraint (Mason, 1959). In addition, androgens may depress plasma levels of glucocorticoids in primates (Brown & Migeon, 1956; Huis in't Veld, Louwerens & van den Spek, 1960). It was therefore decided to study the response of plasma cortisol to ACTH without these neural or hormonal influences. This report describes the effects of ACTH on castrated rhesus monkeys adapted to chronic restraint.
Four chair-restrained, orchidectomized rhesus monkeys (Macaca mulatta) bearing chronic indwelling venous catheters were used as experimental subjects and were housed, maintained and subjected to blood sampling as
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SUMMARY
The rate of aldosterone production in vitro by adrenal glands from rats hypophysectomized 7 days previously, treated with corticotrophin (ACTH) and subjected to dietary sodium restriction for 2 weeks, was decreased 6 h after nephrectomy. However, 18 h and 48 h after nephrectomy there was a marked increase in the rate of aldosterone production in vitro. In addition there was a rise in the plasma potassium concentration. These results indicated that in order to detect whether the influence of growth hormone on aldosterone secretory response to sodium restriction in hypophysectomized rats was mediated by the kidney, studies had to be performed within 6 h after removal of the kidneys.
Since the effect of growth hormone on aldosterone production requires 2 days to develop (Palkovits, de Jong, van der Wal & de Wied, 1971), rats hypophysectomized 54 h previously were used. The kidneys were removed 6 h before decapitation. In these animals, the administration of growth hormone in the presence of ACTH restored the aldosterone secretory response to sodium deficiency.
The results suggest that growth hormone maintains the aldosterone secretory response to sodium restriction in hypophysectomized rats in the absence of the kidneys.
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The influence of adrenalectomy on the level of immunoreactive 18–24 ACTH extracted from hypothalamus, hippocampus and pituitary gland of rats was investigated. Brain ACTH was further characterized by fractionation by gel-permeation chromatography. Porcine 1–39 ACTH was exposed to synaptic plasma membranes in vitro in order to evaluate the role of metabolic conversion in changes of brain ACTH content.
Removal of the adrenals, when compared with sham-adrenalectomy, resulted in a transient depletion of ACTH content in the anterior pituitary gland and the hippocampus, but not in the hypothalamus and the neurointermediate lobe. However, sham-adrenalectomy caused a transient reduction in levels of ACTH when compared with levels before operation in all tissues studied.
The effects of adrenalectomy on hippocampal ACTH content persisted in hypophysectomized rats. Treatment of adrenalectomized rats with corticosterone failed to restore the reduced ACTH content when it was administered in doses that completely suppressed the release of pituitary ACTH. Adrenal steroids, however, may exert a direct effect on the metabolism of ACTH in the brain as judged from the in-vitro studies with porcine 1–39 ACTH exposed to a synaptosomal plasma membrane fraction of hippocampal tissue. The present study suggests that control of brain ACTH occurs independently of the control of pituitary ACTH release.
