Abstract

Pregnancy in subprimate mammals generally requires a pregnancy recognition signal from the conceptus (embryo/fetus and associated membranes) that may be antiluteolyic. Antiluteolytic signals from the conceptuses prevent uterine production of luteolytic pulses of prostaglandin F2α (PGF) that would cause regression of the corpus luteum and its production of progesterone. Progesterone is the hormone of pregnancy and it is required for maintenance of pregnancy in all mammals. Alternatively, a signal from the maternal anterior pituitary (e.g., prolactin) or placenta (chorionic gonadotrophin) may be a luteotrophic signal. Luteotrophic signals act directly to stimulate formation of corpora lutea and their secretion of progesterone which is required for establishment and maintenance of pregnancy, as well as maintenance of a quiescent uterus and birth of a healthy offspring. Parturition, the birth process, occurs with maturation of the hypothalamic-anterior pituitary-adrenal axis of the fetus and production of cortisol by the adrenal cortex of the fetus. Cortisol induces enzymes which metabolize progesterone to estradiol, estradiol induces enzymes that metabolize arachidonic acid to PGF and PGF causes regression of the corpus luteum. Decreasing concentrations of progesterone and increasing concentrations of estrogens increase receptors for oxytocin and PGF on the uterine myometrium and the formation of gap junctions among smooth muscles of the myometrium. This allows oxytocin and PGF to induce coordinated and strong contractions of the myometrium to expel the fetus and placenta during the birth process.

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