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chapter

34

Endocrine Metabolism V: Reproductive System

F I G U R E 3 4 - 6

Placental synthesis of estrogens. The placenta lacks the key enzyme necessary for formation of estrogens from

cholesterol (CYP 17) and relies on androgenic precursors from the maternal and fetal compartments. The major

androgen used comes from the fetal zone of the fetal adrenal; this is DHEAS, which is also taken up and metabolized by

fetal liver into 16«-hydroxy-DHEAS. The placenta converts DHEAS into estrone (Ej) and estradiol (E

2

) and processes

16a-hydroxy-DHEAS into estriol (E

3

). Estrogens enter the maternal circulation and appear in maternal urine as

conjugated estrogens.

resistance that benefits the fetus because it increases the

availability of maternal glucose for fetal consumption. In

the mother, hPL also exerts a prolactin-like effect and, with

estrogen and progesterone, promotes ductal and alveolar

growth in the mammary gland during the third trimester

of pregnancy. However, prolactin is believed to be more

important than hPL in this effect.

Decidual Prolactin

The maternal placenta (decidua basalis) is believed to

produce a hormone that is biologically and antigenically

similar to pituitary prolactin. If released into the amni-

otic fluid during the third trimester of pregnancy, it may

maintain amniotic fluid volume and osmolality.

Relaxin

The maternal placenta also produces relaxin, a hormone

produced by the ovaries. Relaxin causes relaxation of the

cervix during parturition.

Parturition

Precisely what initiates parturition in humans is not

known. Unlike the situation in sheep, there is no induction

of placental CYP 17 by fetal cortisol to bring about a re-

duction in progesterone production and, hence, parturi-

tion. During late gestation, rising levels of estrogen are

thought to increase the synthesis of oxytocin in hypothala-

mic magnocellular neurons to induce oxytocin receptors in

the myometrium and to increase myométrial contractility

by lowering the membrane potential. During this period,

relaxin from the decidua softens the cervix for impending

delivery. At term an unidentified triggering factor in fetal

urine stimulates uterine production of PGE| and PGF2„,

which lead to myométrial contraction, mainly in the fun-

dus, and encourages movement of the infant through the

cervical canal. Dilation of the cervix by the infant stimu-

lates the release of oxytocin by neuroendocrine reflex, fur-

ther stimulating uterine contractions, which in turn causes

more cervical stretching and a positive feedback to oxy-

tocin release, until delivery is complete.

Lactation

During midpregnancy and late pregnancy, growth and dif-

ferentiation of mammary glands are promoted by the com-

bined effects of estrogen, progesterone, and prolactin (or

hPL). In the presence of prolactin or hPL, estrogen stimu-

lates branching of the mammary ducts and increases their