Fig. 14. Interactions between CRH-ACTH-PGs and cortisol in the placenta; influences on the fetal plasma ACTH pool and fetal adrenal steroid output; and mediation by estrogen of uterine sensitivity to oxytocin through increased gene expression for decidual and myometrial oxytocin receptors. Because cortisol paradoxically stimulates placental CRH, a series of forward loops is established. (Challis JRG, Brooks AN: Maturation and activation of hypothalamic-pituitary-adrenal function in fetal sheep. Endocr Rev 10:182, 1989; © The Endocrine Society)