angiogenesis Uterine angiogenesis is upregulated by human chorionic gonadotropin and progesterone and downregulated by estrogen. The balance of influences of progesterone and estrogen determine the state of angiogenesis in the uterus during early pregnancy. Suppression of the maternal immune system High levels of progesterone produced by the embryonic placenta regulate lymphocyte proliferation at the maternal-fetal interface, locally suppressing maternal immune response against the developing embryo. Suppression of GnRH secretion to prevent further follicular maturation Negative feedback of progesterone inhibits hypothalamic pulsatile GnRH neurosecretion, ovulatory GnRH release and pituitary gonadotropin surges thereby effectively preventing further follicular maturation. Preparation of maternal metabolic systems Progesterone regulates metabolism of carbohydrates, proteins, and lipids, resulting in physiological changes associated with pregnancy. The mix of hormones characteristic of early pregnancy promote natural growth of maternal tissues and weight gain. In the second half of pregnancy, progesterone and prolactin prepare the mammary glands for lactation. Preparation of mammary glands for lactation Estrogens and progesterone promote mammary epithelial cell proliferation resulting in the formation of the primary and secondary ductal structure. Progesterone induces formation of tertiary side-branches in the mammary glands during puberty and during the luteal phase of the menstrual cycle upon which lobuloalveolar structures form under the influence of prolactin. Prolactin stimulates lactogenesis. Induction of sleep hCG appears to be soporific during pregnancy; levels of hCG correlate with sleep changes during pregnancy, and administration of hCG increases sleep in rats likely via neuronal LHCGR. References Endocrinology Human reproduction