&NA;Corticotropin releasing hormone (CRH) is produced in intrauterine sites including the placenta, decidua, and myometrium during human pregnancy. Placental CRH may have endocrine, paracrine, and autocrine functions. Its output into the maternal circulation increases as a function of gestation and correlates with increases in levels of mRNA encoding CRH in placental syncytiotrophoblast. Regulation of placental CRH expression and activity is multifactorial, being inhibited by progesterone and nitric oxide (NO), and stimulated by cytokines, neuropeptides, and glucocorticoids. CRH acts as a vasodilator in perfused placental tissuein vitro, may modulate maternal and fetal pituitary function, and has been implicated in mechanisms associated with the onset of labor at term and preterm.