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The potential role of beta-endorphin (beta-EP) as a stimulus to fetal GH, PRL, and chorionic somatomammotropin secretion was investigated in the chronically catheterized ovine fetus. beta-EP (500 microgram/kg, iv) was administered to six fetuses between 84-100 days gestation and to four fetuses between 112-131 days gestation (term, 147 days). The peak incremental GH response of 104.4 +/- 21.1 ng/ml in the younger fetuses was greater (P less than 0.01) than that of the older fetuses (38.0 +/- 11.9 ng/ml). Pretreatment of the fetus with naloxone (100-500 microgram/kg, iv) 5 min before beta-EP reduced (P less than 0.02) the GH response to beta-EP, which suggests that the GH stimulating action of beta-EP was mediated via opiate receptors. Naloxone alone (400 microgram/kg, iv bolus, followed by 400 microgram/kg over 1 h of infusion) had no significant effect on fetal plasma GH. There was no significant change in plasma PRL after beta-EP; however, fetal PRL rose in the three oldest fetuses studied (122, 126, and 131 days). Fetal ovine chorionic somatomammotropin was not altered by either beta-EP or naloxone. The fetal hypothalamic pituitary unit can respond by mid-gestation to exogenous beta-EP with increasing GH secretion. However, in late gestation, the GH responsiveness to beta-EP decreases significantly. It is postulated that this decreased responsiveness is a consequence of the maturation of hypothalamic inhibitory mechanisms regulating GH secretion. The effects of beta-EP on GH and PRL secretion are dissociated in the ovine fetus.
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Gluckman et al. (1980) studied this question.
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