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MAGDA WEISS and I. R. McDONALD

As part of the systematic investigation of adrenal function in marsupials, the following data were obtained from the common wombat (Vombatus hirsutus), a bear-like burrowing marsupial restricted to south-eastern Australia (see Troughton, 1957).

Four wombats, three males and one female weighing 25–30 kg., were anaesthetized with ether, followed by i.v. sodium pentobarbitone. The left adrenal gland, which has a single vein draining into the left renal vein, was exposed through a midline incision. The procedures for collecting adrenal venous blood and steroid assay have been described previously (Weiss & McDonald, 1965). The quantitative estimates were confirmed by measurement of absorbance in u.v. light and Porter-Silber chromogens (Silber & Porter, 1954) for cortisol, and u.v. light absorbance only for corticosterone. To assay tetrahydrocortisol and cortisone, the deproteinized watery fraction of plasma was hydrolysed with β-glucuronidase/aryl sulphatase (Boehringer and Soehne, Mannheim, Germany). The purified extract was chromatographed in system B/50 and the

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M. DALLE and P. DELOST

SUMMARY

Concentrations of cortisol, corticosterone and cortisone in the plasma and adrenal glands, liver glycogen and plasma glucose of foetal, newborn and mother guinea-pigs were estimated during the last 6 days of pregnancy and throughout the first 24 h post partum. At the same time progesterone was measured in the plasma of the mother. During the prepartum rise in foetal plasma cortisol levels and liver glycogen, no significant change in the foetal adrenal cortisol content was observed. The plasma and adrenal cortisol concentrations of the mother were much higher than those observed in the foetus and increased significantly before parturition. In the mother as in the foetus, cortisone and corticosterone represent only a small percentage of corticosteroids compared with cortisol. These results indicate that the autonomous capacity of foetal adrenals, inhibited by maternal secretions before term, appears suddenly at birth.

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J Arola, J Liu, P Heikkila, V Ilvesmaki, K Salmenkivi, R Voutilainen, and AI Kahri

Inhibins are gonadal glycoprotein hormones whose main endocrine function is to inhibit pituitary FSH secretion. In addition to testes and ovaries, other steroid-producing organs are sites of inhibin alpha subunit expression. To study the role of inhibins in human adrenal gland, we screened a panel of 150 adrenals (10 normal adrenals, 25 adrenocortical hyperplasias, 65 adrenocortical adenomas, 30 adrenocortical carcinomas and 20 phaeochromocytomas) for inhibin alpha expression. mRNA levels of inhibin alpha subunit were studied in 57 samples and all tissues were stained immunohistochemically with an inhibin alpha subunit-specific antibody. Inhibin alpha mRNA was detected in all adrenocortical tissues. Virilizing adenomas possessed a 10-fold higher median inhibin alpha mRNA expression than did normal adrenals. Bilaterally and nodularly hyperplastic adrenals and other than virilizing adrenocortical tumours had their median inhibin alpha mRNA levels close to those of normal adrenals. Immunohistochemically, inhibin alpha subunit was detectable in all normal and hyperplastic adrenals, as well as in 73% of the adrenocortical tumours. However, the percentage of inhibin alpha-positive cells varied greatly in different tumour types. The median percentage of positive cells was 10 in non-functional and Conn's adenomas, 30 in Cushing's adenomas and 75 in virilizing adenomas. In malignant adrenocortical tumours the median percentage of inhibin alpha-immunopositive cells was 20 in non-functional carcinomas, 30 in Conn's carcinomas, 65 in Cushing's carcinomas and 75 in virilizing carcinomas. All phaeochromocytomas were negative for inhibin alpha subunit both at the mRNA level and immunohistochemically. Our data show that inhibin alpha subunit is highly expressed in both normal and neoplastic androgen-producing adrenocortical cells, with less expression in cortisol-producing and hardly any in aldosterone-producing cells. This suggests a specific role for inhibins in the regulation of adrenal androgen production. We did not find any significant difference in inhibin alpha expression between benign and malignant adrenocortical tumours. Thus inhibin alpha gene does not seem to have a tumour suppressor role in human adrenal cortex.

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MAGDA WEISS and I. R. McDONALD

SUMMARY

Adrenal venous and peripheral blood was collected from five adult and two immature kangaroos, anaesthetized with pentobarbitone.

Seven C-21 Δ4, 3-oxo steroids were identified in extracts of adrenal venous blood from all animals. The major component—72–92% of detected corticosteroids—was cortisol. The remainder were 11-deoxy and 21-deoxy cortisol, corticosterone, aldosterone, 11β-OH and 17α-OH progesterone. In four out of six experiments, i.v. corticotrophin caused variable degrees of increase in corticosteroid secretion. Maximum cortisol secretion rates in all the adults and the immature male were in the range 29–70 μg./hr./100 mg. adrenal, or 28–58 μg./hr./kg. body weight and 98 μg./hr./100 mg. or 114 μg./hr./kg. in the immature female.

Average aldosterone secretion rate in the adults was 0·27 μg./hr./100 mg. adrenal, or 0·18 μg./hr./kg. body weight. It was significantly higher in the immature male. However, the Na status of the animals was not known.

Cortisol was the major corticosteroid in peripheral blood plasma at concentrations of 2·0–8·1 μg./100 ml.

The unusual secretion of 21-deoxy cortisol suggests there may be differences in some aspects of adrenocortical biosynthesis, compared with eutherians.

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F. A. HARRISON, I. R. McDONALD, and J. Y. F. PATERSON

SUMMARY

The apparent rate of cortisol turnover was determined in conscious and anaesthetized sheep by injection of tritium-labelled cortisol. Simultaneously, the rate of cortisol secretion was determined by collection of adrenal venous blood. The apparent rate of cortisol turnover was found to be two to three times the rate of cortisol secretion.

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R. J. KEYNES, G. W. SMITH, J. D. H. SLATER, M. M. BROWN, S. E. BROWN, N. N. PAYNE, T. P. JOWETT, and C. C. MONGE

Measurements have been made of hormonal changes relevant to salt and water balance during prolonged exposure to hypoxia to improve our understanding of the syndrome of acute mountain sickness. We have attempted to delineate the detailed inter-relationships between the renin–aldosterone and the vasopressin systems by a metabolically controlled study, involving an orthostatic stress (45° head-up tilt) and an injection of a standard dose of ACTH to test adrenal responsiveness. Three Caucasian medical students underwent a 7-day equilibration at 150 m (Lima, Peru), followed by a 6-day sojourn at 4350 m (Cerro de Pasco, Peru) and a final 7 days at 150 m. Measurements were made of sodium and potassium balance, body weight and the 24-h renal excretion of vasopressin, cortisol and aldosterone 18-glucuronide. These variables showed little change, except for that of aldosterone 18-glucuronide, which fell sharply at altitude and rebounded even more sharply on return to sea level. At altitude, basal plasma levels of renin activity and aldosterone fell, and the response to orthostasis was attenuated, but the fall of plasma renin activity, as compared to plasma aldosterone, was delayed; on return to sea level this dissociation was exacerbated with the return of normal renin responsiveness lagging behind that of aldosterone. We suggest that unknown factors which dissociate the orthodox renin–aldosterone relationship, other than the activity of the angiotensin I-converting enzyme, are operative on exposure to hypoxia.

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D. I. FATTAH, B. J. WHITEHOUSE, and G. P. VINSON

Rat adrenal capsules incubated with [3H]18-hydroxydeoxycorticosterone (18-OH-DOC) and [3H]18-hydroxycorticosterone gave appreciable yields of aldosterone from both precursors, similar in size to those obtained from labelled corticosterone, deoxycorticosterone and progesterone under the same conditions. After feeding rats for 14 days on a flour diet deficient in sodium, aldosterone production from endogenous precursors in vitro was increased twofold compared with that by adrenal glands from animals receiving the flour diet with 1% sodium chloride added (control diet). When adrenal capsules from animals on the low-sodium flour diet were incubated with high specific activity [3H]18-OH-DOC (sp. act. 40 Ci/mmol), the yield of [3H]aldosterone was increased two- to threefold compared with that produced by capsules from animals on the control diet. When capsules were incubated with low specific activity [3H] 18-OH-DOC and [14C]corticosterone (sp. act. 52 mCi/mmol) only the yield of [14C]aldosterone was increased. Yields of labelled 18-hydroxycorticosterone from all precursors tested were increased three- to fourfold in animals receiving the low-sodium diet relative to the controls.

The results show that 18-OH-DOC can be an effective precursor for aldosterone formation by rat adrenal capsules, and that production of aldosterone and 18-hydroxycorticosterone from this precursor can be stimulated by a low-sodium diet. This suggests the existence of an alternative pathway for aldosterone biosynthesis involving 18-OH-DOC as an intermediate.

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M. PALKOVITS, W. de JONG, B. van der WAL, and D. de WIED

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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A. SPÄT, J. STURCZ, ÁGNES FARKAS, and Á. FAZEKAS

An important way of examining adrenocortical function is the analysis of adrenal venous blood. In the rat, owing to the small dimensions, direct cannulation of the adrenal vein is not suitable for routine work. Vogt (1954) overcame this obstacle by collecting adrenal venous blood from the left renal vein. However, ligation of the renal pedicle disturbs physiological conditions, and if the kidney plays any role in aldosterone regulation, Vogt's method cannot be considered suitable for experiments on aldosterone secretion.

In order to avoid the disturbance of the renal circulation during the collection of adrenal venous blood, the following method has been developed. After ligation of the renal end of the left adrenal vein, the vessel is opened carefully (but not transsected!). Adrenal venous blood flows without resistance through the aperture into the abdominal cavity. In order to prevent intravascular clotting the animal is heparinized. A reduction in the rate of

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Stephan Werth, Helge Müller-Fielitz, and Walter Raasch

Aldosterone has been identified as an important factor in obesity-associated hypertension. Here, we investigated whether sphingosine-1-phosphate (S1P), which has previously been linked to obesity, increases aldosterone release. S1P-induced aldosterone release was determined in NCI H295R cells in the presence of S1P receptor (S1PR) antagonists. In vivo release of S1P (100–300 µg/kgbw) was investigated in pithed, lean Sprague Dawley (SD) rats, diet-obese spontaneous hypertensive rats (SHRs), as well as in lean or obese Zucker rats. Aldosterone secretion was increased in NCI H295R cells by S1P, the selective S1PR1 agonist SEW2871 and the selective S1PR2 antagonist JTE013. Treatment with the S1PR1 antagonist W146 or fingolimod and the S1PR1/3 antagonist VPbib2319 decreased baseline and/or S1P-stimulated aldosterone release. Compared to saline-treated SD rats, plasma aldosterone increased by ~50 pg/mL after infusing S1P. Baseline levels of S1P and aldosterone were higher in obese than in lean SHRs. Adrenal S1PR expression did not differ between chow- or CD-fed rats that had the highest S1PR1 and lowest S1PR4 levels. S1P induced a short-lasting increase in plasma aldosterone in obese, but not in lean SHRs. However, 2-ANOVA did not demonstrate any difference between lean and obese rats. S1P-induced aldosterone release was also similar between obese and lean Zucker rats. We conclude that S1P is a local regulator of aldosterone production. S1PR1 agonism induces an increase in aldosterone secretion, while stimulating adrenal S1PR2 receptor suppresses aldosterone production. A significant role of S1P in influencing aldosterone secretion in states of obesity seems unlikely.