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The placenta produces GnRH and possesses GnRH receptors, but these receptors have a lower affinity for GnRH than do pituitary GnRH receptors.33 Placental tissue responds to GnRH in vitro through a calcium-mediated second messenger system with increased hCG secretion.46 The immunodetection of GnRH in villous cytotrophoblast cells, the correspondence of the peak of placental hCG secretion with the greatest abundance of villous cytotrophoblast cells relative to syncytiotrophoblast, and the greater responsiveness to GnRH by first trimester placental tissue than by term placenta, are consistent with the idea that cytotrophoblast-derived GnRH governs syncytiotrophoblast hCG secretion.33 However, administration of GnRH to pregnant women does not increase serum hCG levels.47 The failure of exogenous GnRH to affect hCG levels in vivo may be attributed to the fact that placental GnRH receptors have a lower affinity for this releasing factor compared with pituitary GnRH receptors and would not be activated at the concentrations of GnRH administered or because the trophoblast GnRH response systems are saturated by endogenous hormone