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Removal of the corpuscles of Stannius from the European eel (Anguilla anguilla L.) is followed by a fall in the concentration of plasma sodium and a rise in that of potassium and of calcium (Fontaine, 1964; Chester Jones, Henderson & Butler, 1965). It seemed possible that the corpuscles secrete corticosteroids, possibly aldosterone (Fontaine, 1963; Leloup-Hatey, 1964). A large quantity of corpuscles were therefore analysed for steroidogenetic capacity.
Fresh viscera from about 5000 eels, when gutted alive for commercial purposes, were obtained in Billingsgate Market. The corpuscles, a ventral pair on the posterior kidney, were removed in the Department of Zoology, St Bartholomew's Hospital Medical School, where the preliminary experiments were done.
Four experiments were carried out consisting of incubation of chopped corpuscles in a shaking incubator under air at 37° for 3 hr. The medium, isotonic with eel plasma, is given by Sandor et al. (1965). The substrate was a
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SUMMARY
Extracts of human plasma in ethanolic sulphuric acid contain two groups of fluorogens. The fluorescence of one of these increases linearly with time, while the other gives a constant fluorescence between 8 and 20 min. after extraction into the acid mixture. Measurement of the rate of increase in fluorescence of the plasma extracts permits the proportion of the total fluorescence due to the stable component to be calculated.
The component with constant fluorescence probably consists entirely of cortisol and corticosterone. This finding has been used to improve the specificity of a simple method for the determination of adrenal corticosteroids in human plasma. This improved method is described and assessed, and a range of normal values is reported.
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SUMMARY
The mechanism by which combined treatment with monoamine oxidase inhibitors and a corticosteroid reduces the weight of the accessory sex glands in intact rats by about one half has been studied. Phenelzine sulphate in combination with hydrocortisone acetate given for 30 days to ovariectomized rats reduced the pituitary stores of luteinizing hormone (LH) by 33%. Similar reductions in somatotrophic hormone, corticotrophin and thyroid-stimulating hormone content were found after comparable treatment, whereas luteotrophic hormone increased.
The increase of weight of the seminal vesicles and prostate gland produced by human chorionic gonadotrophin could be partly antagonized by the simultaneous administration of mebanazine and dexamethasone, but the action of testosterone on these glands in castrated animals was not inhibited. Interference with the production and effectiveness of LH is therefore the most likely mode of action by which these drugs effect the reduction of the weight of the accessory sex glands.
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Neonatology Division, Diabetes Division, Geriatric Research, Barshop Institute for Longevity and Aging Studies, Department of Obstetrics, Department of Pediatrics
Neonatology Division, Diabetes Division, Geriatric Research, Barshop Institute for Longevity and Aging Studies, Department of Obstetrics, Department of Pediatrics
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Introduction Antenatal corticosteroid administration to pregnant women has become the standard of care for mothers at a risk of delivering a premature infant. Maternal treatment with synthetic glucocorticoids (GCs) decreases the incidence of many
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characterised and cloned in human tissues, 11β-HSD1 and 11β-HSD2 ( Stewart 1996 , White et al. 1997 ). The tissue-specific expression of the isozymes plays a crucial role in corticosteroid physiology by regulating glucocorticoid and mineralocorticoid receptor
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SUMMARY
The changes in plasma ACTH concentration of pregnant sheep and their foetuses during the latter half of pregnancy and during labour were studied. Before 140 days of gestation the mean concentration in foetal arterial plasma was 117 ± 19 (s.e.m.) pg/ml which rose to a mean of 286 ± 63 pg/ml. The rise in ACTH occurred at about the same time as, but not before, the rise in corticosteroid concentration in foetal plasma. The maternal plasma ACTH concentration did not change during the latter half of pregnancy and had a mean concentration of 64 ± 9 pg/ml. During labour there was a progressive rise in the ACTH concentration in foetal plasma which was not associated with any corticosteroid changes. Ethanol did not suppress labour but reduced the ACTH concentration in foetal plasma.
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SUMMARY
Parturition in the guinea-pig is not preceded by any consistent change in the maternal plasma concentrations of progesterone, total unconjugated oestrogens or corticosteroids, or by a significant change in the concentration of progesterone-binding globulin (PBG). The onset of parturition was delayed by high doses of oestrogens (stilboestrol and oestradiol), but was not affected by oestriol or an antiserum raised against oestradiol. Premature parturition was achieved by the intra-carotid infusion of adrenocorticotrophin or prostaglandins (PGF2α, PGE2, I.C.I. 80,996) in conscious animals with indwelling catheters. I.C.I. 80,996, a potent analogue of PGF2α, induced parturition in all seven guinea-pigs treated; delivery occurred within 6 h of starting the infusion in six animals, and within 48 h in the seventh. The undesirable side-effects that accompanied treatment with PGF2α or PGE2 were not encountered with I.C.I. 80,996. Parturition induced experimentally resembled normal delivery but was not preceded by any significant change in the maternal levels of progesterone, total unconjugated oestrogens, corticosteroids, PBG or CBG in the circulation. Oxytocin was not detected until the delivery of the first foetus.
Parturition was not induced by maternal or foetal injections of corticosteroids or dexamethasone. Earlier findings are confirmed that the foetal adrenal grows steadily throughout late pregnancy and, unlike the foetal lamb adrenal, undergoes no rapid phase of growth immediately before term. Foetal adrenal weight decreased relative to foetal body weight.
The trigger for parturition in this species remains unidentified.
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SUMMARY
Using the techniques of equilibrium dialysis at 36 °C and gel filtration at 4 °C, a highaffinity, transcortin-like, corticosteroid binding system has been demonstrated in the blood plasma of the marsupial Trichosurus vulpecula.
The affinity constant for non-albumin binding was 4·018 ± 1·032 × 107 (s.d.) 1/mol for males and 4·046± 0·981 × 107 for females. The concentration of non-albumin binding sites was 1·82 ± 0·76 × 10−7 mol/l in males and 1·86 ± 0·57 × 10−7 mol/l for females. Oestrogen administration, sufficient to cause marked hypertrophy of the genital tract in the females, had no effect on the affinity constant or the concentration of the non-albumin binding sites in either males or females.
The general condition of the animals deteriorated during oestrogen administration and there were significant falls in the concentrations of albumin and cortisol in the blood plasma. In one animal which died during oestrogen treatment, the adrenal glands were significantly hypertrophied.
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Hypothalamic-pituitary-adrenal (HPA) activity is governed by glucocorticoid negative feedback and the magnitude of this signal is determined, in part, by variations in plasma corticosteroid-binding globulin (CBG) capacity. Here, in gonadectomized male rats we examine the extent to which different testosterone replacement levels impact on CBG and HPA function. Compared with gonadectomized rats with low testosterone replacement ( approximately 2 ng/ml), plasma adrenocorticotropin and beta-endorphin/beta-lipotropin responses to restraint stress were reduced in gonadectomized rats with high testosterone replacement ( approximately 5 ng/ml). Plasma CBG levels also varied negatively as a function of testosterone concentration. Moreover, glucocorticoid receptor binding in the liver was elevated by higher testosterone replacement, suggesting that testosterone acts to enhance glucocorticoid suppression of CBG synthesis. Since pituitary intracellular CBG (or transcortin) is derived from plasma, this prompted us to examine whether transcortin binding was similarly responsive to different testosterone replacement levels. Transcortin binding was lower in gonadectomized rats with high plasma testosterone replacement ( approximately 7 ng/ml) than in gonadectomized rats with low testosterone replacement ( approximately 2 ng/ml). This testosterone-dependent decrease in pituitary transcortin was associated, in vitro, with an enhanced nuclear uptake of corticosterone. These findings indicate that the inhibitory effects of testosterone on corticotrope responses to stress may be linked to decrements in plasma and intrapituitary CBG. This could permit greater access of corticosterone to its receptors and enhance glucocorticoid feedback regulation of ACTH release and/or proopiomelanocortin processing.
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ABSTRACT
Steroid-metabolizing enzymes modulate the effects of androgens on brain differentiation and function, but no similar enzymatic system has been demonstrated for adrenocorticosteroids which exert feedback control on the hypothalamus. 11β-Hydroxysteroid dehydrogenase (11β-OHSD) rapidly metabolizes physiological glucocorticoids (corticosterone, cortisol) to inactive products, thereby regulating glucocorticoid access to peripheral mineralocorticoid and glucocorticoid receptors in a site-specific manner. Using in-situ hybridization, we found expression of 11β-OHSD mRNA in neurones of the hypothalamic paraventricular nucleus (PVN) where corticotrophinreleasing factor-41 (CRF-41) is synthesized and from where it is released into hypophysial portal blood. Administration of glycyrrhetinic acid (GE), a potent 11β-OHSD inhibitor, decreased CRF-41 release into hypophysial portal blood in the presence of unchanged circulating glucocorticoid levels, suggesting that 11β-OHSD regulates the effective corticosterone feedback signal to CRF-41 neurones. These effects of GE were not observed in adrenalectomized animals, demonstrating dependence on adrenal products. In contrast, GE led to two- to threefold increases in arginine vasopressin and oxytocin release into portal blood, effects also dependent upon intact adrenal glands. These results suggest that 11β-OHSD in the PVN, and possibly other sites, may represent a novel and important control point of corticosteroid feedback on CRF-41 release in vivo.
Journal of Endocrinology (1993) 136, 471–477
