Fetal endocrine signals and preterm labor

Increased uterine contractility at term and preterm results from activation and then stimulation of the myometrium. Activation can be provoked by mech anical stretch of the uterus and by an endocrine pathway resulting from inc reased activity of the fetal hypothalamic-pituitary-adrenal axis. Cortisol, derived from the fetal adrenal in cases of intrauterine compromise or from the maternal adrenal in response to stress, or generated locally from cort isone in choriodecidual trophoblasts, provides a crucial link to uterine st imulation. Cortisol contributes to the increased production of prostaglandi ns (PGs) by fetal membranes and the decidua through the upregulation of PG synthase and the downregulation of PG dehydrogenase enzymes. Cortisol also stimulates placental corticotropin-releasing hormone (CRH) output, although CRH may both relax and stimulate uterine activity depending on the distrib ution and affinity of its receptor subtypes. Other agents such as cytokines may intercede in this sequence to stimulate PGs and/or CRH, giving rise to a cascade phenomenon that results in preterm birth. Copyright (C) 2001 S. Karger AG. Basel.