[“Noncompetitive Inhibitor

Another important hormone regulating luteal function is PRL.In rodents, the Methscopolamine proestrus surge of circulating PRL in a nonfertile cycle induces luteolysis, but after pseudopregnancy or pregnancy, the increase in systemic PRL promotes the survival and function of the corpus luteum, including both proangiogenic and antiangiogenic effects.Treatment with PRL induces endothelial cell proliferation in the corpus luteum of cycling rats, D-Cycloserine whereas reducing circulating PRL levels with bromocriptine interferes with corpus luteum angiogenesis.There is good evidence that estrogen drives VEGF production and angiogenesis during the proliferative phase of the cycle, whereas the presence and the absence of progesterone have been implicated in endometrial angiogenesis during the secretory and postmenstrual phases of the cycle, respectively. Other hormones involved in endometrial angiogenesis include chorionic gonadotropin and ANG II. Systemic PRL derived from the anterior pituitary gland increases during proestrus and early pregnancy in rodents, whereas in humans, circulating PRL remains low during the menstrual cycle and gradually increases during gestation, reaching its maximum level at term, a specialized endometrial stromal tissue that differentiates in the luteal phase of the menstrual cycle and throughout pregnancy.The location and temporal presence of PRL suggest its inuence on endometrial angiogenesis during the secretory phase of the cycle and at the time of implantation and early placental development. Consistent with this, pharmacologically induced hyperprolactinemia enhances endometrial thickness. PRL receptors are localized in the decidua, cytotrophoblasts, synciotriotrophoblasts, which are important cellular sources of proangiogenic factors like VEGF, placental growth factor, bFGF, and angiopoietins. Also, the placenta produces GH and PL, both of which promote endometrial gland proliferation and can activate PRL receptors.On the other hand, cyclic changes in the activity of the RAS also occur during the reproductive cycle and are reected in the circulation and in the expression of all of its components in the uteroplacental unit. During the luteal phase, ANG II increases in stromal cells near endometrial spiral arterioles, and ANG II receptor expression is increased in endometrial glands and blood vessels, ANG II may contribute to the vasopressor mechanism that initiates menstruation, causing hypoxiainduced regression and degradation of upper endometrial tissue in response to the withdrawal of progesterone. Also, a role for ANG II in endometrium regeneration is suggested by the presence of ANG II and ANG II receptors in endometrial glandular and stromal cells during the proliferative phase. During pregnancy, all the components of RAS are active in the placenta, and increased ANG II levels in the maternal circulation are associated with placental angiogenesis and elevated blood ow. This effect is relevant, as vasodilation of maternal systemic circulation and the increased blood ow within the fetoplacental unit are major adaptations of mammalian pregnancy, and systemic and renal ANG. The different components of the KKS have also been identied in the cycling, suggesting that BK and its receptors actively participate in increased uterine blood ow, vasopermeability, and angiogenesis.In addition to proangiogenic mechanisms, antiangiogenic events operate to regulate the regional distribution of placental neovascularization. Antiangiogenic mechanisms maintain the avascular nature of the decidual layer immediately surrounding the synciotrophoblastic mass of the invading embryo.

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