Initiation of parturition in the goat: evidence for control by foetal glucocorticoid through activation of placental C21-steroid 17alpha-hydroxylase.

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-17beta rose. The concentration of cortisol in the foetus was low at dexamethasone-induced delivery. Metabolism of pregnenolone, progesterone, 17alpha-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 placenta obtained before the onset of labour (or from animals induced to kid by administration of prostaglandins), the main product of progesterone metabolism was a 5beta-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 17alpha-hydroxylate and progesterone was metabolized to 5beta-pregnane-3alpha/3beta,17alpha,20alpha-triols and 17alpha,20alpha-dihydroxypregn-4-en-3-one. The appearance of placental 17alpha-hydroxylase was correlated with raised maternal concentrations of 17alpha,20alpha-dihydroxypregn-4-en-3-one and androstenedione. The induction or activation of placental 17alpha-hydroxylase may represent the mechanism by which foetal glucocorticoid controls the onset of labour in the goat.