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ABSTRACT
The effects of chronic infusion of porcine relaxin on oxytocin release were studied in lactating rats. Infusion of relaxin (4·2 μg/h for either 4 or 6 days) suppressed reflex milk ejection and reduced litter weight gain for 48 h compared with saline-infused controls. After 2 days, neither the rate of growth nor the frequency of milk ejection were significantly different from controls. For 24 h after the infusion of relaxin ended, litters gained weight more quickly than controls but there was no difference seen in the frequency of milk ejection. The effects on oxytocin release of stopping an infusion of relaxin after 3 days were investigated. There was a significant (P <0·01) rise in plasma oxytocin (up to 90 pmol/l) 30 min after the infusion was stopped, followed by a sustained rise in intramammary pressure. Treatment of relaxin-infused rats with naloxone (0·1 mg/kg) when the infusion was halted caused a more rapid release of oxytocin (within 2 min), a greater release of oxytocin (up to 140 pmol/l) and a prolonged rise in intramammary pressure.
J. Endocr. (1987) 114, 241–246
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ABSTRACT
Experiments were carried out to investigate the effects of porcine relaxin on the course of gestation and delivery in the rat. Plasma relaxin was maintained at approximately 600 nmol/l from day 19 to day 23 of gestation by i.v. infusion from chronically implanted minipumps. Relaxin significantly (P<0·001) prolonged the length of gestation in 17 rats compared with controls, without causing dystocia or affecting the number of live births. Six rats gave birth during relaxin infusion. In these animals there was a significant (P<0·001) increase in the interval between successive deliveries compared with control animals, resulting in prolonged labour. The remaining 11 rats gave birth after the infusion was completed, when the interval between successive deliveries was significantly (P< 0·025) shorter than controls. The results are consistent with the hypothesis that relaxin has a central action suppressing the release of oxytocin as well as a peripheral action on the myometrium and cervix.
J. Endocr. (1986) 109, 85–88
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ABSTRACT
Experiments were carried out to establish whether infusion of relaxin prolongs gestation and labour in the rat by suppressing release of oxytocin, and whether the effects of relaxin on birth could be reversed by the opioid antagonist naloxone. Female rats were implanted with subcutaneous osmotic minipumps for the infusion of purified porcine relaxin into the jugular vein for 84 h from either day 19 or day 20 of gestation. Infusion of relaxin delayed the onset of labour and in those animals which delivered during relaxin infusion, delivery was longer by approximately 45 min. Plasma oxytocin levels 40 min after delivery of the first fetus were 45·25 ± 3·6 pmol/l (mean ± s.d.) in unoperated controls and significantly (P < 0·01) depressed (23·89 ± 3·9) in rats that delivered during infusion of relaxin. Rats that delivered after the infusion of relaxin had finished, gave birth significantly (P < 0·05) faster than controls and plasma oxytocin levels were significantly (P < 0·01) raised (77·87 ±15·9 pmol/l). Naloxone treatment (1 mg/kg; i.m.) given immediately after the delivery of the first fetus reversed the inhibitory effect of relaxin and the interval between successive deliveries was slightly faster than that of controls. Plasma oxytocin levels in relaxin-infused naloxone-treated rats were significantly (P < 0·01) higher than values in unoperated control rats. The results confirm that relaxin suppresses oxytocin release possibly through an opioid system and this may be important in the control of the timing of birth.
J. Endocr. (1986) 111, 99–102
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ABSTRACT
In our colony of female rats (220–320 g body weight) undergoing regular 4-day oestrous cycles there were significant, marked rises in concentrations of LH, FSH and prolactin between 09.00 and 19.00 h on pro-oestrus.
The i.p. injection of difluoromethylornithine (DFMO; 40–400 mg/kg), a specific inhibitor of the activity of ornithine decarboxylase, at 15.00 h on prooestrus had a differential effect on the rise in plasma concentrations of the various hormones thereafter. The drug produced a significant, partial, dose-related suppression of the rise in plasma concentrations of LH and prolactin, but had no significant effect on the rise in FSH.
For time-course studies, 120 mg DFMO/kg were injected at 13.00, 15.00 or 17.00 h and groups of animals killed at 19.00 h. Only the injection at 15.00 h was effective in causing a significant reduction in plasma concentrations of LH and prolactin at 19.00 h. Pituitary content of the hormones was found to be unaffected by the administration of DFMO at the times and doses tested.
These results suggest that DFMO has a selective inhibitory effect on enhanced LH and prolactin secretion on the afternoon of pro-oestrus in the rat, whilst not affecting FSH release. There seems to be a limited time (after 13.00 but before 17.00 h) during which its administration is effective.
Journal of Endocrinology (1989) 121, 495–499
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ABSTRACT
Corticotrophin-releasing hormone (CRH) is produced by both the placenta and fetal membranes at term in man, and CRH mRNA has been detected in human placental tissue. The synthesis of CRH and its control during early pregnancy, however, have not been established, and the role of CRH produced in the placenta and fetal membranes is not known.
We examined whether amnion and placental tissue obtained between 12 and 15 weeks of gestation produced CRH in vitro, whether steroid modulation of output occurred and whether CRH affected prostaglandin (PG) output by the placenta and amnion.
Immunoreactive (ir) CRH output by amnion (2·8 ± 0·31 (s.e.m.) nmol/105 cells) was significantly (P<0·01) greater than that from placenta (1·76 ± 0·21 nmol/105 cells). Output of ir-CRH decreased in the presence of progesterone, but increased in the presence of cortisol and dexamethasone. There was no significant effect of progesterone or ir-CRH output by placental cells; however, ir-CRH output was increased in the presence of dexamethasone and cortisol. There was no significant effect of corticosterone on ir-CRH output by either amnion or placental cells. Both ACTH and CRH stimulated the output of PGE2 and PGF2α by amnion cells. In contrast, there was no significant effect of PGE2 output by placental cells maintained in the presence of either human CRH or ACTH. Output of PGF2α by placental cells was increased in the presence of both CRH and ACTH.
We conclude that both amnion and placental tissue produce CRH in early gestation, and that this output is modulated by steroids. CRH and ACTH stimulate PG output by amnion and placenta in early pregnancy, raising the possibility of local (autocrine and paracrine) interrelations in vivo.
Journal of Endocrinology (1990) 125, 153–159
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The 'spontaneous' development of pituitary tumours has been studied in the Wistar–Furth strain of rat. In females aged 64–135 weeks the incidence was as high as 69% whereas in males aged 72–116 weeks only 6% developed tumours. Hyperprolactinaemia was invariably associated with these spontaneous pituitary tumours but excessive secretion of growth hormone (GH) was found in one animal only. Bromocriptine inhibited secretion of prolactin and DNA synthesis of the tumours. In a mixed GH- and prolactin-secreting tumour transplanted to a peripheral site, bromocriptine reduced the size of the tumour as well as the secretion of both hormones. Oestradiol reversed the inhibitory action of bromocriptine on prolactin secretion and tumour growth but failed to influence the reduction in GH secretion caused by the drug.
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SUMMARY
Rat pituitary tumours of the GH3 cell line, secreting growth hormone (GH), were induced to grow in Wistar–Furth rats and the effect of prolonged excessive secretion of GH on various organs was investigated. Total body weight of the tumour-bearing animals increased by over 100% compared with control animals and there was widespread visceromegaly affecting especially the liver, kidney, spleen and adrenals. The heart was also considerably enlarged. The effects of excessive GH on skeletal muscle were not uniform and, using a histochemical technique, it was found that the size of type 1 muscle fibres was increased to the greatest extent whereas fibre type 2A was unaffected. Synthesis of DNA in the heart and skeletal muscle was also increased in tumour-bearing animals. Removal of the tumours was followed by a considerable regression in the size of most organs, although hypertrophy of the heart was affected least by a return to normal plasma levels of GH. It was concluded that animals bearing GH3 cell tumours provide a useful experimental model for the study of the tissue changes in acromegaly.
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The effect of bromocriptine on hormone secretion and the growth of the prolactin- and growth hormone (GH)-secreting rat pituitary tumour of the GH3 cell line has been compared with that of ergotamine and other ergot alkaloids. Bromocriptine in doses ranging from 1 to 20 mg/kg had no effect on tumour growth or on the excessive secretion of GH by the tumour; prolactin concentrations were reduced only by the highest dosage of the drug. Similarly the tumour was resistant to the administration of ergocryptine, ergocornine and the synthetic ergolines, lergotrile and CH 29–717. In contrast, ergotamine reduced secretion of both GH and prolactin and considerably inhibited the growth of the tumour. Experiments in vitro showed that ergotamine inhibited DNA synthesis of the tumour cells and decreased hormone secretion. It was concluded that ergotamine had a direct inhibitory action on the GH3 cell tumour which was not mediated through the dopaminergic mechanisms.
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ABSTRACT
Experiments were carried out on anaesthetized, lactating rats to investigate the possible role of the subfornical organ in mediating relaxin-induced inhibition of reflex milk ejection. Milk ejection was judged by the behavioural response of the sucklings and by transient rises in intramammary pressure. Radiofrequency lesions of the subfornical organ, or control lesions in adjacent areas of the cerebrum, did not affect the pattern or the magnitude of intramammary pressure changes at reflex milk ejection. Purified porcine relaxin given by either i.v. (5 μg) or intracerebroventricular (50 ng) injection suppressed reflex milk ejection in intact, sham-lesioned and control-lesioned rats, but had no effect on either the pattern or magnitude of reflex milk ejection in rats with lesions of the subfornical organ. The subfornical organ, which is situated at the interface between the blood, brain and the cerebrospinal fluid appears to mediate, at least in part, the relaxin-induced inhibition of reflex milk ejection in the rat.
J. Endocr. (1987) 115, 347–353
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ABSTRACT
Prolactin secretion by a human pituitary tumour cell line produced in our laboratory was stimulated by TRH, vasoactive intestinal peptide (VIP) and epithelial growth factor (EGF). All raised the intracellular concentration of free calcium (Ca2+ i) of cells loaded with a fluorescent quinoline Ca2+ indicator in suspension, but the effect of TRH was much more rapid and less prolonged than that of VIP and EGF. Both TRH and VIP also increased Ca2+ i in GH3 rat pituitary tumour cells, but in this cell line the effect of VIP was only found in attached cells grown on cover-slips. In both human and rat cell lines, the increase in Ca2+ i produced by TRH was independent of extracellular calcium, whereas this was a requirement for the action of VIP and EGF. It is concluded that the prolactin secretogogues, VIP and probably EGF, increase Ca2+ i through an effect on plasma membrane calcium channels and that this effect differs from that of TRH.
J. Endocr. (1987) 114, 119–123