Influence of acute administration of human growth hormone and alpha-MSH on plasma concentrations of aldosterone, cortisol, corticosterone and growth hormone in man.

The effect of acute administration of human growth hormone (HGH) and of alpha-melanocyte stimulating hormone (alpha-MSH) on plasma aldosterone, cortisol, corticosterone and growth hormone has been studied in normal man and in patients with panhypopituitarism. There is no acute effect of exogenous HGH on plasma levels of aldosterone, cortisol and corticosterone in normal man and in patients with panhypopituitarism. The plasma level of immunoreactive HGH measured during acute HGH infusion in man does not seem to be proportional to the dose administred in our study. Alpha-MSH raises the concentartion of plasma HGH, BYT THIS STIMULATION IS NOT DOSE-DEPENDENT. Aldosterone, cortisol and corticosterone concentrations are not influenced by the elevation of HGH mediated by alpha-MSH in normal man. Although in some patients with panhypopituitarism an elevation of plasma aldosterone concenntration following alpha-MSH infusion is observed, it is unlikely that MSH is directly involved in the acute regulation of aldosterone secretion in healthy subjects.     

Perinatal changes in plasma and adrenal corticosterone and aldosterone concentrations in the mouse

The concentrations of corticosterone and aldosterone in the plasma and adrenal glands of foetal, newborn and mother mice were estimated during the last 4 days of pregnancy and throughout the perinatal period. The level of corticosterone in the maternal and foetal plasma fell from day 17 of gestation until birth, and then remained stable. Whereas the corticosterone content of the maternal adrenal glands did not change significantly, that of the foetal adrenal glands reached a peak on day 19 of gestation. At every stage of gestation, the level of corticosterone in the maternal plasma was higher than that in the foetus. Changes in the concentration of aldosterone in the foetal plasma and adrenal glands were similar and characterized by peak values at birth. In the mother during the last 4 days of pregnancy, the level of aldosterone in the plasma was higher than in non-pregnant mice, but lower than that in the foetus.     

Seasonal changes in plasma and adrenal concentrations of cortisol,corticosterone, aldosterone,and electrolytes in the adult male sand rat (Psammomys obesus)

Seasonal changes in adrenocortical function were studied in the adult male sand rat (Psammomys obesus) live-trapped in the region of Béni-Abbès in the Algerian Sahara Desert. Cortisol was found to be the primary corticosteroid secreted in the sand rat. Plasma and adrenal concentrations of cortisol, corticosterone, and aldosterone exhibited marked significant annual variations mainly characterized by a decline during spring, a minimum in early summer, and an increase in autumn. In spite of the high sodium intake of this animal in the field, the aldosterone levels seemed similar to those of other mammals. Plasma sodium and potassium concentrations were relatively high in Psammomys obesus (respectively, about 150 and 8 mM) and, except for a slight increase in early summer, varied little throughout the year.     

Propranolol enhances the effect of ACTH on plasma cortisol, but not on aldosterone in man

An accidental observation led to the suspicion that propranolol (P) enhances the effect of exogenous ACTH on plasma cortisol. To examine this matter further, large-dose ACTH tests (25 IU im) were performed in 10 normal young males: i) without treatment (n =10); ii) after 11/2 days of P treatment (n = 10); iii) after 11/2 days of metoprolol treatment (n = 6). Six other subjects received infusions of 0.2 IU of ACTH/hour for 12 h: i) without pretreatment; ii) after 11/2 days of P treatment. P pretreatment (80 mg t.i.d.) led to a small but significant decrease in plasma cortisol (9.4 +/- 0.8 micrograms/100 mg; mean +/- SE, vs. 11.3 +/- 0.7 micrograms/100 ml in controls). The maximum percentage increase of plasma cortisol after ACTH injection was 383% +/- 35% (mean +/- SE) after P and 253% +/- 22% in controls (p less than 0.05). The enhancement of the absolute and relative increase of plasma cortisol after ACTH injection seems to be mainly due to lowering of basal cortisol levels, since the effect of ACTH on plasma cortisol in normal subjects in inversely related to basal cortisol. The effect of metoprolol on basal cortisol and the cortisol response to ACTH was less pronounced than that of P. In the long-term-infusion study the effect of P was less apparent than in the acute study. P had no significant effect on basal plasma aldosterone or on the aldosterone response to ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute effects of digoxin on plasma aldosterone and cortisol in monkeys

Digoxin, a cardiac glycoside, is used to increase cardiac contractility via inhibition of Na⁺/K⁺-adenosinetriphosphatase (ATPase) and increase intracellular calcium in congestive heart failure. Inhibitory effects of digoxin have been demonstrated on the biosynthesis of gonadal hormones and adrenal glucocorticoids in rats. However, acute effects of digoxin on levels of adrenal corticosteroid hormones in the primates in vivo are uncertain. Therefore, we test the hypothesis that a single injection of digoxin decreases the secretion of aldosterone and cortisol in monkeys. An intravenous injection of digoxin (1 μg/kg) inhibited basal and adrenocorticotropin (ACTH)- or KCl-stimulated aldosterone release in monkeys. Furthermore, digoxin induced a decrease in ACTH- and KCl-stimulated cortisol release. Administration of digoxin did not alter plasma concentrations of Na⁺ and K⁺. Ouabain, a selective inhibitor of Na⁺/K⁺-ATPase, did not affect ACTH- or KCl-stimulated aldosterone and cortisol release. These results revealed that injection of digoxin induced an inhibitory effect on aldosterone and cortisol secretion in monkeys. Because ouabain did not affect levels of plasma aldosterone or cortisol, we suggest that (1) the Na⁺/K⁺-ATPase pathway may not be involved in the mechanism of action of digoxin on aldosterone or cortisol secretion in monkeys and/or (2) the Na⁺/K⁺-ATPase is more sensitive to digoxin than to ouabain in monkeys.     

Prolonged infusions of Ile5-angiotensin-II in sodium replete and deplete man: effects on aldosterone, ACTH, cortisol, blood pressure, and electrolyte balance.

Angiotensin II (Ile5) was infused for 72 h into 4 sodium replete (3 ng/kg/min) and 8 sodium deplete (3 or 6 ng/kg/min) healthy young men after appropriate control periods, and the effects on aldosterone secretion, plasma cortisol, ACTH, renin activity, plasma and urinary electrolytes, and blood pressure were assessed. Sustained contrived elevation of plasma angiotensin II levels in sodium replete subjects to the range of moderate sodium depletion led to a sustained increase in plasma and urinary aldosterone levels, which further and significantly increased between the 1st and 2nd days of angiotensin II infusion, when gross sodium retention during infusion was prevented. This additional increase may be explained as the expression of a "trophic" effect of angiotension II on the zona glomerulosa. In the sodium deplete state, the absolute increment of aldosterone secretion for a given elevation of angiotensin II levels diring infusion was larger than in sodium replete subjects. This confirms the conclusions from previous short-term angiotensin II infusion experiments that sodium deficiency sensitizes the zona glomerulosa against angiotensin II. The "trophic" effect of angiotensin II on the adrenal gland seems to be one mechanism by which the sensitization is brought about, but insufficient for its full explanation. Since plasma ACTH and cortisol, plasma sodium and potassium concentrations, and potassium blance did not change significantly across sodium depletion or angiotensin II infusion, the mechanism of sensitization awaits its full elucidation. The effect of angiotensin II on blood pressure was blunted by soidum depletion. The opposite shifts in sensitivity against angiotensin II of the zona glomerulosa and of resistance blood vessels with changes in the sodium state seem to be an effective and important means in the regulation of body sodium.     

Measurement of cortisol, cortisone, 11-deoxycortisol and corticosterone in foetal sheep plasma during the perinatal period.

A method is described for the resolution and individual quantitation of cortisol, cortisone, 11-deoxycortisol and corticosterone in foetal sheep plasma. The steroids were extracted by solvent partition and separated by LH-20 Sephadex column chromatography. Radioimmunoassay was used for the measurement of 11-deoxycortisol and cortisone and competitive protein-binding for corticosterone and cortisol. The relative levels of these steroids in the plasma of chronically catheterized sheep foetuses from 12 days before birth to term and then in the newborn lamb until 2 days of age are recorded. Cortisol gradually increased from a basal concentration of between 0 - 5 and 3 - 0 mug/100 ml plasma between days 12 and 5 pre partum, and then rose rapidly to 10 mug/100 ml plasma during the last 5 days of pregnancy to reach a maximum during or just after birth. Two days post partum the levels had fallen to approximately 3 mug/100 ml plasma. The mean value for 11-deoxycortisol between days 8 and 3 pre partum was 0 - 4 mug/100 ml plasma and increased in the final days before delivery to 1 - 0 mug/100 ml. Corticosterone initially showed slightly higher levels (approximately 1 - 5 mug/100 ml) in the earlier period of investigation but then fell during the immediate pre-partum period to 0 - 8 mug/100 ml. Cortisone was not detected at any stage of the investigations. The relationship between levels of cortisol and 11-deoxycortisol in foetal plasma and myometrial contractility is shown. An increase in uterine activity was seen to occur at the time that cortisol levels were at their maximum. The 11-deoxycortisol values throughout this particular study remained low. The results are discussed in relation to recorded levels in the adult and to previous studies in vitro with regard to changing steroid biosynthetic enzyme activity.