INITIATION OF PARTURITION IN THE GOAT: EVIDENCE FOR CONTROL BY FOETAL GLUCOCORTICOID THROUGH ACTIVATION OF PLACENTAL C21-STEROID 17α-HYDROXYLASE

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Abstract
Infusion of dexamethasone into chronically catheterized foetal kids induced delivery in 41–65 h. Changes in the concentrations of placental and ovarian steroids in the maternal circulation at dexamethasone-induced delivery mimicked those preceding spontaneous kidding at term; in both instances the peripheral concentration of progesterone fell and the concentration of oestradiol-17β rose. The concentration of cortisol in the foetus was low at dexamethasone-induced delivery. Metabolism of pregnenolone, progesterone, 17α-hydroxyprogesterone and androst-4-ene-3,17-dione by extracts of foetal placenta was investigated in late pregnancy, after premature parturition induced with dexamethasone or prostaglandins and after spontaneous parturition at term. In placentae obtained before the onset of labour (or from animals induced to kid by administration of prostaglandins), the main product of progesterone metabolism was a 5β-pregnane-3,20-diol. In contrast, placentae from animals in which the foetal level of glucocorticoid had been raised (after spontaneous parturition or by administration of dexamethasone to the foetus) were able to 17α-hydroxylate and progesterone was metabolized to 5β-pregnane-3α/3β,17α,20α-triols and 17α,20α-dihydroxypregn-4-en-3-one. The appearance of placental 17α-hydroxylase was correlated with raised maternal concentrations of 17α,20α-dihydroxypregn-4-en-3-one and androstenedione. The induction or activation of placental 17α-hydroxylase may represent the mechanism by which foetal glucocorticoid controls the onset of labour in the goat.