Pituitary hormone analogs and their effects
During gestation, placental tissue secretes a range of substances whose physiological action is analogous to the mother's pituitary hormones. This broad functional group includes human chorionic gonadotropin (hCG), placental lactogen (PL), adrenocorticotropic hormone (ACTH), and chorionic somatomammotropin, which is a direct functional analog of growth hormone.
In the maternal body, these biologically active substances effectively complement pituitary function. A crucial role of hCG and placental lactogen is supporting the corpus luteum: they continuously stimulate its growth and secretory activity in early pregnancy. This continues until the placenta is fully formed and begins independently producing steroid hormones. Furthermore, on the surface of chorionic villi, these hormones provide vital immunosuppression, suppressing the immune responses of the maternal organism and thereby preventing immunological rejection of the embryo.
In the developing fetus, human chorionic gonadotropin acts as a potent stimulator: it triggers the production of its own ACTH and corticosteroids directly within the cells of the embryonic adrenal cortex.
Female sex hormones (Steroids)
Normally, in a non-pregnant woman, the synthesis of sex steroids occurs in the ovaries. However, during pregnancy, the ovaries become functionally inactive. This is because new follicles do not develop, so estrogens are not produced, and the corpus luteum eventually undergoes natural regression, completely ceasing progesterone production.
The placenta takes on this massive compensatory function. It begins to secrete required amounts of estrogens and progesterone, maintaining an optimal hormonal balance. For the fetus, the presence of estrogens is of absolute critical importance, as they exhibit a pronounced mitogenic effect—that is, they strongly stimulate cell division processes, ensuring the continuous growth of all embryonic tissues.
Relaxin and preparation for labor
In late pregnancy, the synthesis of a specific hormone—relaxin—acquires special functional significance. The main physiological goal of this substance is the comprehensive preparation of the female body for safe and natural childbirth.
Under the systemic influence of relaxin, large-scale structural changes occur in the tissues of the birth canal: the cervix significantly softens and dilates. The hormone also induces relaxation of the pubic symphysis and the pelvic ligamentous apparatus, which critically facilitates the passage of the fetus. Concurrently, relaxin effectively inhibits premature contractions of the smooth musculature of the uterus (myometrium), reliably preventing the early onset of labor.
Briefly: answers to topical questions
At what week of pregnancy does the placenta completely take over progesterone synthesis from the corpus luteum?
The placenta takes over progesterone synthesis from the corpus luteum after the 1st trimester (at the end of the first 3 months of pregnancy). The exact week is not specified in the sources.
Early in pregnancy, the hormone is produced mainly by the corpus luteum (corpus luteum). After the first trimester, it undergoes involution, and subsequent synthesis is entirely assumed by the placenta. The resulting placental progesterone enters the maternal bloodstream predominantly.
Which specific placental cells synthesize human chorionic gonadotropin and placental lactogen?
Human chorionic gonadotropin is synthesized by trophoblast cells, specifically its inner layer—cytotrophoblast. The specific cell type producing placental lactogen is not specified; it is only known that it is produced exclusively in the placenta.
- Human chorionic gonadotropin — produced by the cytotrophoblast (the source of initial hormone production during implantation).
- Placental lactogen — synthesized only in the placenta; present in low concentrations in amniotic fluid.
From which precursor substances does the placenta synthesize estrogens?
The placenta synthesizes estrogens from fetal adrenal androgens. Since the ovaries are functionally inactive during pregnancy and do not produce estrogens, the placenta takes over this compensatory function.
- Estrogens — steroid hormones synthesized by the syncytiotrophoblast of chorionic villi using androgen precursors from the fetus.
Their active synthesis begins from the middle of pregnancy, and estrogen levels serve as an indicator of placental function.
HPR-H (hCG, Estrogens, Progesterone, Relaxin) — the four main placental hormones delivering a happy end (safe and healthy delivery).
Class and exam questions
Why is the placenta called a temporary analog of the pituitary gland and ovaries?
Because during pregnancy it takes over their functions by synthesizing pituitary hormone analogs (hCG, PL, ACTH, somatomammotropin) and female sex steroids (estrogens, progesterone), thereby fully compensating for ovarian inactivity.
What role does human chorionic gonadotropin (hCG) play in early pregnancy?
hCG, together with placental lactogen, actively supports the secretory function and growth of the corpus luteum until the placenta reaches maturity and begins independently producing steroid hormones in the required volume.
Why does the placenta need an immunosuppression function?
The immunosuppressive action of placental hormones in the area of chorionic villi is critically necessary to suppress the maternal immune response, which prevents the immunological rejection of the genetically half-foreign fetus.
How do placental estrogens affect the developing fetus?
Estrogens, intensively produced by the placenta, exert a strong mitogenic effect on the fetus, directly stimulating cell division and ensuring the growth of embryonic tissues.
What else to study on this topic
- Mechanisms of local immunosuppression on the surface of chorionic villi.
- The effect of human chorionic gonadotropin on the development of the fetal adrenal cortex.
- The process of corpus luteum regression and the transition of steroidogenesis to the placenta.
- The mitogenic effect of estrogens at the cellular level in the embryo.
- The effect of relaxin on myometrial smooth muscle cells.
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