The process of reproduction in the mammalian female involves interactions between gonadal and placental steroids and, possibly, protein hormones such as placental lactogen, and the uterine endometrium. These interactions are discussed relative to available data from pigs and with the understanding that the concepts presented may not be directly applicable to other species. Swine embryos enter the uterus for continued development beyond the early blastocyst stage and, within the uterus, the spherical blastocyst, of about 2 mm diameter on day 12, undergoes rapid elongation to an organism of about 1 m in length by day 15 of pregnancy. During this period of elongation, the blastocyst appears to provide the chemical signal, presumably unconjugated estrogens, that allows for corpora lutea (CL) maintenance (luteostatic effect) and, therefore, continued production of progesterone by the CL which is essential for pregnancy. Estrogens from the blastocyst may exert their luteostatic effect on the uterus by causing prostaglandin F2 alpha, the presumed porcine uterine luteolysin, to be secreted in an exocrine (toward the uterine lumen) rather than an endocrine (toward the endometrial stroma and vasculature) direction during pregnancy. Consequently, prostaglandin F2 alpha is sequestered in the uterine lumen and does not become available, via the utero-ovarian vasculature, to exert its luteolytic effect. The potential steroid precursor(s) available to the trophoblast for estrogen synthesis appear to be produced through endometrial conversion of progesterone to unconjugated androgens, e.g., androstenedione and testosterone, and conjugated estrogens, e.g., estrone-sulfate and estradiol-sulfate. The estrogens may, in concert with progesterone and possibly other hormones, placental lactogen for example, act locally, i.e., at the site of placentation to: result in a luteostatic effect; increase uterine blood flow; enhance water, electrolyte and substrate (carbohydrate and amino acid) transport to the site of placentation and across the placenta; affect synthesis and secretion of macro-molecules (histotroph) by the uterine glands that serve as enzymes and (or) carrier molecules and control or modulate physiological and (or) biochemical events essential to placental and fetal development that are not understood.