Human trophoblast produce GnRH and its precursor, immunologically and chemically identical to those of hypothalamic origin. Placental GnRH stimulates human chorionic gonadotropin secretion by the syncytiotrophoblast. It is known that GnRH analogue has negative effect on early rat pregnancy and may cause abortion through its action on the corpus luteum. A significant reduction of progesterone production was found in pregnant rats treated with GnRH agonist. GnRH caused a significant decrease in the maximal contraction intensity of non-pregnant and pregnant uterine muscle strip, following the action of oxytocin and acetylcholine. It was observed that treatment of pregnant rat with pharmacological doses of GnRH was able to delay parturition. Experimentally, GnRH significantly inhibited the release of placental prostaglandins E and F and thromboxane B 2 in a dose dependent fashion. Maternal circulating GnRH levels at 25-35 weeks of gestation were significantly higher in women who later had post-term pregnancies. In an other study maternal circulating GnRH concentration was found to be significantly lower in four patients who developed preterm labor and delivery. Low doses of GnRH in pregnant rats produced inhibition of postpartum lordosis behavior.