Embryonic steroid synthesis and luteal oxytocin production: controlling mechanisms for the maternal recognition of pregnancy.

In both pigs and sheep in early pregnancy the function of the corpora lutea is maintained beyond the normal time of luteal regression. The mechanism by which this is brought about appears in both species to involve reduced uterine secretion of the uterine luteolysin, prostaglandin F2 alpha, as a result of the secretion of an embryonic antiluteolysin. In the pig this antiluteolysin is an oestrogen, and in the sheep, the protein trophoblastin. Loss of luteal oxytocin also occurs in sheep early in pregnancy, and this may contribute to reduced luteolytic drive during the period between 25 and 50 days of gestation when the embryonic antiluteolysin is absent. Concentrations of oxytocin in the corpora lutea appear to be controlled by a factor of uterine origin, since luteal oxytocin is also depleted after hysterectomy.