Estrogen regulates the timing of implantation in the mouse and serves as the conceptus signal for corpora lutea maintenance and establishment of pregnancy in the pig. Although the type of implantation and source of estrogen differ, synthesis and release of estrogen from either the ovary (rodents) or conceptus (pig) initiates a series of uterine responses that permit trophoblast adhesion and attachment to the uterine lumenal epithelium for invasive implantation in the rodent or non-invasive diffuse implantation/placentation in the pig. Estrogen stimulates secretion of many factors involved with uterine remodeling, vascular permeability and angiogenesis, alterations in the uterine glycocalyx, and tolerance of the maternal immune system to the fetal allograft. Many uterine responses to the conceptus resemble an acute inflammatory phase response. Presence of the kallikrein-kininogen-kinin system in the rodent and pig suggest that the release of kinins into the uterus plays a significant role in altering uterine receptivity and conceptus implantation. In the pig, estrogen from the conceptuses initiates a program of inflammatory-like responses and alters the uterine surface glycocalyx for trophoblast adhesion. Although estrogen clearly is essential for normal conceptus development and survival, it can also function as an endocrine disruptor if presented to the uterus at an inappropriate time prior to implantation. Premature and inappropriate estrogen stimulation of the uterus by environmental estrogens or estrogen agonists causes complete embryonic loss in pigs. Environmental and pollutant hormone mimics that alter human and animal health, as well as reproductive function, are a major health concern.