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ABSTRACT
Cortisol kinetics were examined in brook trout (Salvelinus fontinalis) to assess possible relationships with body fluid distribution during acclimation to sea water (SW). The disappearance curve of [3H]cortisol in plasma, after a bolus injection, was analysed by compartmental analysis using a three-pool mammillary model. The results indicated that only ∼ 10% of the total exchangeable cortisol was located in the plasma pool. Over 75% of the total cortisol was associated with a large slowly exchanging pool and the remaining cortisol was located in a second extravascular tissue pool which was in rapid exchange with the plasma pool.
Two days after transfer of trout from fresh water to SW, when plasma chloride concentration was at a new steady state, body weight, intracellular fluid volume, haematocrit and inulin clearance rate were lowered but plasma, blood and extracellular volumes were unaltered. Cortisol plasma clearance rate was unaltered but plasma cortisol concentration, cortisol secretion rate, total cortisol pool size and interpool transport rates were increased. These results are consistent with an acute role for cortisol in SW adaptation of brook trout.
The fraction of the total cortisol cleared was smaller and the average time that cortisol spent in the tissue pools was slightly longer in trout after transfer to SW, possibly reflecting altered fluid dynamics. The fractional disappearance rate was larger at higher plasma cortisol concentrations in the SW trout. This relationship is compatible with the hypothesis that cortisol protein binding protects cortisol from metabolism.
J. Endocr. (1985) 107, 57–69
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, with gestational decreases in vasoactive hormones such as angiotensin II (AII), increases in growth-promoting hormones such as insulin-like growth factors (IGF) and maturational hormones such as cortisol and thyroid hormones; most are magnitudes higher
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(RAAS; Henriksen 2007 , Ostergren 2007 ) and dysregulation of the hypothalamic–pituitary–adrenal axis with resulting increments in basal plasma cortisol levels ( Bruehl et al . 2007 ) and enhanced tissue sensitivity to cortisol ( Andrews et al . 2002
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Human plasma contains similar free concentrations of the active steroid cortisol and its inactive metabolite cortisone. Interconversion of cortisol and cortisone (or corticosterone and 11-dehydrocorticosterone in rats) has been recognized since the 1950s. Until recently it was thought that separate NADP/NADPH-dependent enzymes were responsible: 11β-dehydrogenase to convert cortisol to cortisone and 11β-reductase for the reverse reaction (Abramowitz, Branchaud & Murphy, 1982; Lakshmi & Monder, 1985). It is now known that both activities can be expressed from the same cDNA clone (Agarwal, Monder, Eckstein & White, 1989; Agarwal, TusieLuna, Monder & White, 1990), suggesting that a single 11β-hydroxysteroid dehydrogenase protein (11β-OHSD) catalyses both reactions. Recently, interest in the enzyme was stimulated by observations in patients with congenital 11β-dehydrogenase deficiency (the syndrome of apparent mineralocorticoid excess) (Ulick, Levine, Gunczler et al. 1979; Stewart, Corrie, Shackleton & Edwards, 1988) and in volunteers given the 11β-dehydrogenase inhibitors liquorice (Stewart, Valentino, Wallace et al
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University of Oxford, Nuffield Institute for Medical Research, and Department of Obstetrics and Gynaecology, John Radcliffe Hospital, Headington, Oxford, 0X3 9DS
(Received 10 July 1975)
In sheep and man, parturition is preceded by an increase in the concentration of cortisol in foetal plasma and amniotic fluid respectively (Bassett & Thorburn, 1969; Fencl & Tulchinsky, 1975; Murphy, Patrick & Denton, 1975). In man it has been suggested that cortisol may influence the production of surface active lipids in the foetal lung (see Avery, 1975) and that the foetal adrenal, like that of the sheep, may play a role in the initiation of parturition (see review by Challis & Thorburn, 1975). Because experimental studies are not feasible in man, an animal model would be useful for studies designed to understand the mechanisms and significance of hormonal changes before parturition. We have examined amniotic fluid and maternal plasma cortisol concentrations serially in the
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Glucocorticoids secreted by the foetal adrenal cortex play a major causative role in initiating parturition in the sheep and goat (Liggins, 1968, 1969a; Bassett & Thorburn, 1969; Comline, Nathanielsz, Paisey & Silver, 1970; Thorburn, Nicol, Bassett, Shutt & Cox, 1972). However, Liggins (1969b) failed to precipitate premature parturition with dexamethasone (4 mg/h) infused into the maternal circulation of the pregnant ewe. Fylling (1971) produced delivery with 6–10 mg dexamethasone/day in the pregnant ewe. Since it is uncertain what role glucocorticoids may play in polytocous species, an attempt was made to initiate parturition by infusing cortisol into the maternal circulation of the pregnant rabbit. Cortisol was chosen as the glucocorticoid for infusion since in the newborn rabbit the plasma cortisol: corticosterone ratio is about 3·0 (K. W. Malinowska, R. N. Hardy & P. W. Nathanielsz, unpublished observations).
Pregnant rabbits of known gestational age were anaesthetized with sodium pentobarbitone (30–45
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SUMMARY
Tritium-labelled cortisol was injected intravenously, as a single dose, in 12 experiments on seven sheep with autotransplanted left adrenal glands, in which cortisol secretion rate could be measured directly by sampling adrenal venous blood.
In all experiments, curves which represented sums of two exponential terms could be fitted to the estimates of specific activity of plasma cortisol. The interpretation of the data was based on the distribution of cortisol in two miscible pools, and the calculated rates of cortisol turnover were much greater than the cortisol secretion rates which were measured directly and simultaneously.
Simultaneous injection of Evans blue suggested that 1–2 min. was needed for complete mixing of the injected dose in plasma, during which time labelled cortisol leaves plasma with a half-time of about 1 min. It is concluded that such conditions do not provide a satisfactory basis for tracer kinetic analysis.
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igf1 and igf2 gene expression by GH, insulin, and cortisol, and the effects of insulin and cortisol on GH sensitivity in primary cultured hepatocytes of a cichlid teleost, the Mozambique tilapia ( Oreochromis mossambicus ). Materials and Methods
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Recent reports have demonstrated that plasma testosterone shows a significant diurnal variation, with an early morning peak (Resko & Eik-Nes, 1966; Faiman & Winter, 1971; Okamoto, Setaishi, Nakagawa, Horiuchi, Moriya & Itoh, 1971). Testosterone has also been reported to fluctuate during sleep, possibly associated with rapid eye movement episodes (Evans, MacLean, Ismail & Love, 1971). Thus testosterone, like cortisol (Hellman, Nakada, Curti, Weitzman, Kream, Roffwarg, Ellman, Fukushima & Gallagher, 1970; Krieger, Allen, Rizzo & Krieger, 1971) may be secreted episodically.
In a recent study of ten young men, aged 19–23 yr, who were closely observed while participating in their usual daily routines, plasma samples were drawn approximately every 90 min during the day and night from indwelling catheters. Cortisol was analysed in all samples by the method of Murphy (1968), and testosterone was analysed in all men every 6 h by a modification of the method of Mayes & Nugent
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It is well established that primary and secondary deficiency of cortisol secretion by the adrenals causes a grossly impaired diuresis during the first 4 h after an oral water load, and that the levels of blood cortisol affect the osmotic threshold for secretion of antidiuretic hormone (ADH) by the neurohypophysis (Aubrey, Nankin, Moses & Streeten, 1965). The changes in blood cortisol concentration after a water load, however, have been less thoroughly studied, though Hatfield & Shuster (1959) found a fall in plasma cortisol levels, as measured by the Porter—Silber reaction. Since a variation in cortisol concentration might itself affect diuresis after a water load, such a response would be important in the understanding of the physiology of diuresis and was, therefore, re-investigated.
The experiments were performed on six healthy adult male subjects. No food or fluids were taken from 22.00 h the previous night. At 09.15 h a sample of
