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1. No alteration in cerebral water content was observed in rats following administration of cortisol, aldosterone or the adrenal inhibitor 2 methyl-1,2-di-3′ pyridylpropan-1-one (SU 4885).

2. Aldosterone was found to decrease the cerebral oedema produced by intravenous injection of water.

3. Cortisol and SU 4885 had no effect on cerebral water content following intravenous administration of water.

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Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.

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In hypophysectomized-nephrectomized dogs after intravenous injection of histamine, a marked increase was observed in the rate of secretion of aldosterone, although it was smaller than that in intact dogs. Hypophysectomy plus bilateral nephrectomy greatly impaired the secretion of corticosterone and cortisol in the dog in response to histamine. However, a small yet significant increase in corticosterone and cortisol secretion was observed in hypophysectomized-nephrectomized dogs after intravenous injection of histamine. Additional experiments showed that plasma concentrations of potassium and sodium in hypophysectomized-nephrectomized dogs remained unchanged after intravenous injection of histamine. These results suggest that histamine stimulates aldosterone secretion in the dog partly by a direct effect on the adrenal cortical cells, whereas the effect of histamine on corticosterone and cortisol secretion is mediated mainly, but not totally, by pituitary release of ACTH.

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Comparisons of aldosterone responses to [des-Asp1]-angiotensin II and angiotensin II, often at single dose levels, have shown a wide range of potency ratios. Therefore four-point dose–response comparisons were performed in sodium-replete sheep, using i.v. infusion rates of angiotension II and angiotensin II amide that reproduced the physiological range of blood concentration of angiotensin II for sheep. Angiotensin III was infused i.v. at the same rates. Effects on arterial blood pressure, cortisol secretion rate, adrenal blood flow and plasma levels of Na+ and K+ were also compared. The potency ratio, angiotensin III: angiotensin II amide, was 0·87 for actual aldosterone secretion rate and 0·90 for the calculated increase in aldosterone secretion. For angiotensin III: angiotensin II the ratios were 0·80 and 0·91 respectively. These ratios were not significantly different from 1·00 but the tendency for angiotensin II to be slightly more potent was probably due to a contribution from derived angiotensin III during infusion of angiotensin II. Angiotensin II or angiotensin II amide was ∼ four times as potent as angiotensin III in raising arterial blood pressure. Cortisol secretion rate was slightly but significantly increased by all peptides at the higher infusion rates. Infusions had no effect on adrenal blood flow or plasma levels of Na + but raised plasma levels of K + slightly. These results confirm the conclusion from adrenal arterial infusion experiments that angiotensin II and III are almost equipotent in stimulating aldosterone secretion in sheep.

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T. C. LEE, B. van der WAL, and D. de WIED


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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The metabolism of 11-deoxycorticosterone (DOC) in vitro by homogenates of adrenal glands from various species has been studied.

Homogenates of 'non-fatty' adrenal glands, especially those prepared from golden hamster adrenals, were shown to possess an active 19-hydroxylating enzyme system. In the case of the golden hamster adrenal, approximately 30% of the added DOC was converted to 19-hydroxy-11-deoxycorticosterone (19-OH-DOC). Negligible transformation was observed using homogenates prepared from 'fatty' adrenal glands, similar to the type found in man. 19-OH-DOC was, however, formed from DOC by a homogenate of a human foetal adrenal gland.

No relationship was observed between the 11β-hydroxylating activity of the adrenal homogenate, and the reported cortisol/corticosterone ratio found in the adrenal venous blood of various animals.

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Aldosterone production by isolated adrenal glomerulosa cells from the rat was estimated in the presence of varying concentrations of sodium ion. The reduction of sodium concentration by 5–20 mmol/l, with or without osmotic changes, did not influence the rate of aldosterone production. Aldosterone response to angiotensin II was not modified by varying the sodium concentration.

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P. Soszynski, J. Slowinska-Srzednicka, A. Kasperlik-Zaluska, and S. Zgliczynski


In order to investigate the effect of chronic hypercortisolaemia on endogenous natriuretic factors (atrial natriuretic hormone (ANH) and the Na+/K+ pump inhibitor) digitalis-like substance (DLS), and their relation to hypertension, 28 patients with pituitary-or adrenal-dependent Cushing's syndrome and six patients on high-dose prednisone treatment were studied. Plasma ANH levels were increased in patients with Cushing's syndrome (36·0±1·4 (s.e.m.) ng/l) compared with those in healthy controls (28·6±1·3 ng/l, P <0·01). In prednisone-treated patients, ANH levels (43·8±4·5 ng/l) were higher than those in patients with Cushing's syndrome and in controls (P <0·05 and P <0·01 respectively). DLS measured by radioimmunoassay and binding of [3H]ouabain to erythrocytes was not altered in patients with hypercortisolaemia. Slightly decreased DLS activity in the erythrocyte 86Rb uptake inhibition assay was found in patients with Cushing's syndrome (52·9±2·7%) compared with that in controls (60·9±1·8%, P <0·02). With the exception of cortisol (r = 0·52, P<0·01), none of the other factors determined correlated with the mean arterial pressure in patients with Cushing's syndrome.

Thus, a chronic excess of endogenous and exogenous glucocorticoids increases plasma levels of ANH, but does not substantially influence DLS activity or plasma levels. Neither natriuretic factor is directly related to hypertension in Cushing's syndrome.

Journal of Endocrinology (1991) 129, 453–458

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T. J. McKenna and S. K. Cunningham

While it is well established that aldosterone arises exclusively from the zona glomerulosa of the adrenal gland under the dominant control of the renin-angiotensin system and that cortisol arises from both the zona fasciculata and zona reticularis under the almost exclusive control of adrenocorticotrophin (ACTH), the mechanisms controlling adrenal androgen secretion, predominantly from the zona reticularis, have not been established and are the subject of intense debate. Undoubtedly ACTH plays an important role in the stimulation of adrenal androgen secretion. However, the many instances of dissociation between cortisol and androgen secretion suggest that while ACTH is necessary for androgen biosynthesis, alone it is probably not sufficient. The fetal adrenal secretes Δ5 androgens in abundance; the steroid pattern changing in the early neonatal phase of life to favour Δ4 glucocorticoids with very little androgen production (De Peretti & Forest, 1976). This pattern is maintained into the second half of

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D. T. BAIRD, A. UNO, and J. C. MELBY

There are very few reports of the concentration of androgens (e.g. Weinheimer, Oertel, Leppla, Baise & Bette, 1965) and oestrogens (Engel, 1962) in adrenal venous blood collected from unanaesthetized subjects. Adrenal venous blood was collected by retrograde catheterization of the right or left adrenal vein via the femoral vein in conscious subjects (Spark, Dale, Kahn & Melby, 1969). In each case a control sample was collected by allowing a free drip from a heparinized adrenal catheter. Fifteen min. after the injection of 0·25 mg. β1–24 corticotrophin (ACTH) (Cortrosyn, Organon) into a peripheral vein a further sample of adrenal venous blood was collected.

Cortisol, aldosterone and 18-hydroxycorticosterone were measured as previously described (Spark et al. 1969). Testosterone, androstenedione, oestrone and oestradiol-17β were analysed on a second portion of plasma by double isotope derivative methods (Riondel, Tait, Gut, Tait, Joachim & Little, 1963; Horton, 1965; Baird, 1968). The blanks of the