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SUMMARY
A method of estimating the peripheral plasma concentration of 11-deoxycorticosterone (DOC) in man by means of gas-liquid chromatography with electron capture detection is described. Purification requirements for samples and chromatographic media have been simplified by the use of a detector bypass valve which reduces the risk of detector contamination. For this reason the method is relatively short. There was no measurable blank using either plasma from an adrenalectomized subject or water. The normal range was found to lie between 4·1 and 17·2 ng/100 ml (mean 9·8). Dexamethasone administration to one subject resulted in a subnormal plasma DOC concentration.
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ABSTRACT
Administration of pregnant mare serum gonadotrophin (PMSG) to peripubertal rats, aged 27 days, induces ovulation provided the animals weigh more than 60 g at the time of the injection. In an attempt to determine whether the apparent immaturity of the ovaries in smaller rats is associated with an inability of the pituitary gland to secrete LH, the biological and immunological properties of LH in peripubertal PMSG-treated rats were examined. A single injection of PMSG caused a marked hypersecretion of LH in rats aged 27 days. The LH in the plasma of rats weighing more than 60 g was active in both the radioimmunoassay and the cytochemical bioassay but that in smaller rats was active only in the former. Plasma from both groups of rats stimulated the release of testosterone from dispersed Leydig cells.
Luteinizing hormone-releasing hormone stimulated the secretion, in vitro, of immunoreactive, cytochemically active LH by pituitary tissue from rats weighing over 60 g. The LH released in vitro from tissue from the smaller animals, like that in their plasma, was active in the radioimmunoassay but not in the cytochemical system. The results suggest that an abrupt change in the nature of LH occurs at puberty and that ovulatory cycles commence only when the pituitary gland secretes the adult form of LH with a full spectrum of biological activity.
J. Endocr. (1985) 104, 173–177
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Radioimmunoassay measurements of α-melanotrophin in plasma have identified a diurnal rhythm in male rats. Animals maintained on a 12 h light: 12 h darkness photoperiod had raised levels of plasma α-melanotrophin during the dark phase. Time-series analysis gave a fitted mean level of α-melanotrophin of 52·4 pmol/l, an amplitude of 12·1 pmol/l and peak levels 2·2 h before dawn.
Measurements throughout the oestrous cycle in female rats showed that similar variations between the dark and light phases occurred on the 2 days of dioestrus. The raised levels during the dark period were, however, absent on the nights of pro-oestrus and oestrus. During this pro-oestrous/oestrous period, plasma α-melanotrophin levels were below average but higher than the normal minimum levels found during the light period.
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SUMMARY
Serotonin (5HT, 100 mg/kg) given subcutaneously between 16.00 and 18.00 h on the day of pro-oestrus, at 17.00 h on day 2 of dioestrus and at 13.00 and 17.00 h on day 1 of dioestrus, inhibited ovulation in adult rats. It was ineffective at 13.00 h on the day of pro-oestrus and on day 2 of dioestrus. The anti-ovulatory effect at 17.00 h during pro-oestrus was reversed by pretreatment with 2–4 mg progesterone or 2·5 mg dipyridamole/kg. The effect at 17.00 h on day 2 of dioestrus was reversed by 2 μg oestradiol benzoate. Subcutaneous injection of 5HT antagonized the ovulatory action of exogenous luteinizing hormone and inhibited the passage of 22Na into ovary, uterus and muscle but not the pituitary. Intraventricular administration of 5HT (200 μg/rat) between 13.00 and 18.00 h during pro-oestrus had no effect on ovulation. These results suggest that subcutaneous administration of 5HT does not inhibit ovulation at a central site, but acts as a peripheral vasoconstrictor preventing the passage of hormones to their target organs.
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SUMMARY
The output of oestriol and of pregnanediol during normal pregnancy varies considerably from day to day. This variability detracts from the clinical value of these assays. The variability is reduced if urine collections are made for longer periods of time but such long collections have little clinical application. An attempt was made to reduce the high variability of 4 hr. urine collections by standardizing conditions such as rate of urine secretion, posture and activity. The results of such 4-hourly 'steady state' collections were compared with the results obtained from corresponding 24 hr. and 48 hr. collections. It was concluded that under standardized conditions the 4 hr. collection was very little more variable than the 24 hr. one and gave comparable results.
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α-Melanotrophin was detected by radioimmunoassay in the pituitary glands of fetal rats from day 17 of gestation. The pituitary content of α-melanotrophin increased regularly, at a gradually decreasing rate, throughout gestation and in the postnatal period. Concentrations of α-melanotrophin in the plasma of fetal and newborn rats were below the detection limit of the radioimmunoassay (10 pmol/l). Detectable concentrations were first found in young rats on day 3 after birth and did not differ significantly from those in their mothers throughout the period of suckling. Plasma concentrations of α-melanotrophin were raised in pregnant rats during the last 4 days of gestation and after parturition. They returned to basal levels in the 2 weeks after delivery. After weaning at 3 weeks of age, a large increase in the plasma concentration of α-melanotrophin was detected in juvenile rats. Plasma levels had returned to the normal adult range by 6 weeks of age. The increases in α-melanotrophin in the blood were thought to be the result of non-specific stress effects. The data did not provide evidence for a role for α-melanotrophin in reproductive processes in the rat.
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ABSTRACT
This review emphasizes the heterogeneous structure of the gonadotrophin hormones and the influence of different oligosaccharide structures on the bioactivity of these hormones. A summary has been made of the changes in biopotency of the gonadotrophins throughout the life-cycle of the human and in different endocrine states in the rat.
In general it appears that the charge of the gonadotrophin conferred by the acid radicals attached to the terminal groups on the oligosaccharide structures strongly influences biopotency. Basic structures have a greater potency in in-vitro assays, but a short half-life in the circulation, while acidic isoforms are less potent, but have a longer circulatory time and are thus more active in in-vivo estimations. More basic forms are secreted over the adult reproductive years compared with the prepubertal period and old age. The glycosyl structure of the carbohydrate groups also alters in different endocrine states and is probably also important for the bioactivity and potency of the hormone.
Gonadotrophin-releasing hormone (GnRH) and gonadal steroids can influence the type of isoform synthesized and released, and therefore affect the function of gonadotrophins. GnRH enhances glycosylation, sulphation and biopotency. Oestradiol potentiates the glycosylation induced by GnRH and reduces sialylation, while testosterone increases sialylation.
Journal of Endocrinology (1990) 125, 3–14
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Abstract
Experiments were done to study the effects of porcine relaxin on osmotically evoked changes in intramammary pressure and the release of oxytocin and vasopressin in anaesthetized rats. Injections (1 μ1) of hypertonic (0·75 m) NaCl into the left lateral cerebral ventricle were used to induce consistent rises in intramammary pressure and the release of oxytocin and vasopressin. Plasma hormone concentration was determined by radioimmunoassay. Relaxin (5 μg i.v.) significantly (P<0·05) suppressed the intramammary pressure response to osmotic challenge 5 and 10 min after treatment. However, pretreatment with a specific vasopressin V1 receptor antagonist completely negated the effect of relaxin on intramammary pressure. Baseline levels of oxytocin and vasopressin in unstimulated rats were 41 ± 1·6 and 36±1·1 pmol/l respectively. Osmotic challenge induced significant (P<0·05) rises in plasma levels of both hormones (62·8 ±1·1 and 67·9 ± 1·2 pmol/l respectively) which were further augmented by relaxin (81·3±1·8 and 117·1 ±2·4 pmol/l respectively; P<0·05). The data confirm that central osmotic challenge provokes the release of oxytocin and vasopressin but the effects of oxytocin at the level of the mammary gland may be obscured by the action of vasopressin affecting blood flow to the gland.
Journalof Endocrinology (1994) 141, 75–80
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*A.R.C. Institute of Animal Physiology, Babraham, Cambridge, CB2 4AT, and ‡Department of Physiology, Royal Veterinary College, London, NW1 OTU
(Received 28 March 1978)
Ovulation can be induced precociously in the prepubertal female rat by the administration of pregnant mare serum gonadotrophin (PMSG), provided that the animal weighs over 60 g (Wilson, Endersby & McDonald, 1974). The hormonal changes brought about by this treatment have been studied (J. C. Buckingham, M. B. ter Haar, A. S. McNeilly & C. A. Wilson, data to be published) and it has been found that the preovulatory concentrations of radioimmunoassayable luteinizing hormone (LH) varied according to the antiserum used. These findings are described in the present communication.
Female Sprague–Dawley rats (Tuck & Sons, Rayleigh, Essex) were brought into the department on day 21 of life, kept under conditions of controlled lighting (lights on 05.00–19.00 h) and provided with pelleted rat diet (No. 86, Dixon &
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ABSTRACT
Rat liver exhibits a reversed sexual dimorphism of its two endogenous soluble carbonic anhydrase (CA) isozymes, CA II and CA III. Normal males have hepatic CA III concentrations ten–twenty times those in the female, while female liver contains two–three times more CA II than the male. Hypophysectomy abolishes this sexual differentiation, having no effect on male liver but producing isozyme concentrations in the female liver similar to those in the male. Infusion of a continuous level of GH into male rats induces a female-like isozyme pattern for both CA II and CA III.
J. Endocr. (1986) 110, 123–126
