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ABSTRACT
It has been suggested that melanin concentrating hormone (MCH) possesses potent corticotrophin (ACTH) inhibitory activity, on the basis of the inhibitory effects displayed by salmon MCH on ACTH release from either trout or rat isolated pituitary fragments. Recently, rat MCH has been characterised, and this prompted us to investigate the putative inhibitory activity of synthetic rat MCH on basal and stimulated ACTH secretion from freshly-dispersed rat pituitary cells or incubated rat pituitary fragments, as well on KCl (28 mmol/l) or noradrenaline-evoked release of corticotrophin releasing hormone-41 (CRH-41) from rat hypothalamic explants in vitro. There were no effects of rat MCH on either CRH-41 or ACTH release in vitro.
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ABSTRACT
Six normal male subjects were given, in single blind random order on six separate occasions, i.v. bolus doses of synthetic ovine corticotrophin-releasing factor-41 (oCRF-41; 25 and 50 μg) with and without adrenaline (3 μg/min) i.v. for 150 min, the adrenaline infusions alone and saline placebo. The adrenaline infusions resulted in plasma adrenaline concentrations of 4·33 ± 0·82 (s.e.m.) nmol/l and were associated with an increase in blood glucose, heart rate and systolic blood pressure and a reduction of diastolic blood pressure. Despite these evident biological effects at several sites, there was no stimulation of plasma ACTH or cortisol by adrenaline in comparison with the effect of saline, and no enhancement of the stimulatory effect of either dose of oCRF-41 on ACTH or cortisol secretion. The ACTH response to 50 μg oCRF-41 was greater than that to 25 μg, indicating that the 25 μg dose of oCRF-41 was sub-maximal and capable of further enhancement. As the plasma adrenaline concentrations during the adrenaline infusions reached the upper limit of the physiological range of plasma adrenaline in man, yet failed to enhance the ACTH or cortisol responses to a sub-maximal dose of oCRF-41, we conclude that circulating adrenaline neither exerts a direct stimulatory effect on pituitary corticotrophs nor enhances the effect of CRF under physiological circumstances. The adrenaline infusions attenuated the ACTH and cortisol responses to oCRF-41 and were associated with a transient reduction of basal concentrations of both hormones.
J. Endocr. (1987) 112, 145–150
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ABSTRACT
A specific binding protein for human corticotrophin-releasing hormone (hCRH), which does not bind to the ovine hormone (oCRH), has recently been demonstrated in human plasma. No such binding protein has been found in sheep plasma. We have investigated the half-life of human and ovine CRH in man and in sheep. Peptides were measured directly in plasma with two-site immunoradiometric assays, as these assays are unaffected by the presence of inactivated peptide fragments. In man, the half-life of hCRH (30·5 ± 3·3 min; mean ± s.e.m.) was significantly (P < 0·001) less than that of oCRH (42·8 ± 6·4 min). In sheep, there was no significant difference between the half-life of hCRH (46·5 ± 7·2 min) and that of oCRH (39·8 ± 10·1 min); these half-lives were also significantly (P < 0·001) longer than that of hCRH in man. One possible explanation for the shorter half-life of hCRH in man is that the clearance of hCRH is enhanced by CRH-binding protein, although other binding proteins often have the opposite effect.
Peak ACTH and cortisol responses occurred earlier in sheep than in man, although no differences were found in the response times to oCRH or hCRH within either species. The responses were more sustained in sheep than in man, and the previously reported biphasic response was only seen in some of the sheep and not in man. Absolute responses to either peptide were greater in sheep than in man; however, in man an 8·1-fold rise in ACTH was measured in response to oCRH, while hCRH gave a significantly (P = 0·043) smaller 4·4-fold response. These experiments are discussed with particular reference to the effect of hCRH-binding protein and its possible role in potentiating the clearance of the peptide.
Journal of Endocrinology (1992) 133, 487–495
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ABSTRACT
A synthetic 29-amino acid analogue of human pancreatic GH-releasing hormone (GHRH(1–29)NH2) has recently been shown to stimulate the release of GH in normal subjects. We have studied the GH response to GHRH(1–29)NH2 in nine children irradiated for brain and nasopharyngeal tumours, who were not growing and were deficient in GH as assessed by insulin-induced hypoglycaemia. Serum GH rose in response to GHRH(1–29)NH2 in all the children, and in five the peak serum GH response was > 20 mu./l. The data suggest that when hypothalamo-pituitary irradiation results in GH deficiency, this is due to a failure of the synthesis or delivery of endogenous GH RH from the hypothalamus to the pituitary cells. It also suggests that it may be possible to treat such children using synthetic GHRH in place of exogenous GH.
J. Endocr. (1986) 108, 25–29
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SUMMARY
The distribution of radioactivity after intrajugular injection of l-[3H]prolyl-l-leucyl-glycinamide has been studied by whole-body autoradiography in the mouse and by direct measurement of radioactivity in individual organs of the rat. There is good agreement between results obtained with the two techniques and animal species. High levels of radioactivity were found in the pineal gland, anterior pituitary, posterior (including intermediate) lobe of the pituitary, and epididymal and brown fat. Lower uptake of radioactivity occurred in the submaxillary gland, kidney, and adrenal gland. The preferential uptake of radioactivity by the pineal gland after injection of the labelled tripeptide suggests a role for this hypothalamic hormone in the control of pineal activity.
