Interaction between oxytocin and prostaglandin F2α, during luteal regression and early pregnancy in sheep

The pulsatile release of oxytocin from the corpus luteum in the sheep is responsible for the pulsatile release of prostaglandin F2α (PGF2a) from the uterus at luteolysis. It has been proposed that PGF2aalso reinforces this process by stimulating the release of oxytocin from the corpus luteum. It is, however, unlikely that PGF2a is the major stimulus for oxytocin release at this time. Although thestimulus for the pulsatile release of oxytocin from the corpus luteum appears to reach the ovary fromthe peripheral circulation, the nature of the stimulus is unknown. Pulses of oxytocin originatingfrom the corpus luteum have also been observed during early pregnancy, but the release of PGF2a, inresponse to this signal, is abrogated in some way by ovine trophoblast protein-1 (oTP-1). This proteinhas been shown to inhibit endometrial prostaglandin production and to decrease the amount of PGF2cireleased in response to oxytocin. Reduction of uterine oxytocin receptor concentrations by conceptussecretory proteins or by interferons related to oTP-1 remains equivocal. Inhibition of uterine oxytocinreceptors is, however, probably the major mechanism that prevents luteal regression during earlypregnancy. In cyclic sheep the specific inhibition of uterine oxytocin receptors by l-deamino-2-D-Try(oET)-4-Thr-8-Orn-oxytocin (CAP), a synthetic oxytocin receptor antagonist, inhibits luteal regressionand suppresses pulsatile, but not basal, secretion of uterine PGF2a. Thus, the effects of CAP directlyparallel the endocrinological changes that occur in early pregnancy in the sheep.