Placental growth hormone-which difers from pituitary growth hormone by 13 amino acid residues-is secreted by syncytiotrophoblast in a nonpulsatile fashion (Newbern, 2011). Its regulation and physiological efects are incompletely understood, but it inluences fetal growth via up regulation of insulin-like growth factor 1 (IGF-1). Higher levels have been linked with development of preeclampsia (MinaI, 2007; PerezIbave, 2014). Further, placental expression correlates positively with birthweight but negatively with fetal-growth restriction (Koutsaki, 201l). Maternal serum levels are associated with uterine artery resistance changes (Schiessl, 2007). hat said, fetal growth still progresses in the complete absence of this hormone. Although not absolutely essential, the hormone may act in concert with placental lactogen to regulate fetal growth (Newbern, 2011).
Maternal plasma prolactin levels increase markedly during normal pregnancy. Concentrations are usually tenfold greater at term-about 150 ng/mL-compared with those of nonpregnant women. Paradoxically, plasma concentrations drop after delivery even in women who are breastfeeding. During early lactation, pulsatile bursts of prolactin secretion are a response to suckling.
The principal function of maternal prolactin is to ensure lac tation. Early in pregnancy, prolactin acts to initiate DNA syn thesis and mitosis of glandular epithelial cells and presecretory alveolar cells of the breast. Prolactin also augments the number of estrogen and prolactin receptors in these cells. Finally, pro lactin promotes mammary alveolar cell RNA synthesis, galac topoiesis, and production of casein, lactalbumin, lactose, and lipids (Andersen, 1982). A woman with isolated prolactin dei ciency failed to lactate after two pregnancies (Kauppila, 1987).
This establishes prolactin as a requisite for lactation but not for pregnancy. Grattan (2015) has reviewed the numerous physi ological roles of prolactin for facilitating maternal adaptations to pregnancy. A possible role is proposed for a prolactin frag ment in the genesis of peripartum cardiomyopathy (Chap. 49, p. 963) (Cunningham, 2012).
Prolactin is present in amnionic fluid in high concen trations. Levels of up to 10,000 ng/mL are found at 20 to 26 weeks' gestation. Thereafter, levels decline and reach a nadir after 34 weeks. Uterine decidua is the synthesis site of prolactin found in amnionic luid. Although the exact function of amni onic luid prolactin is unknown, impaired water transfer from the fetus into the maternal compartment to thereby prevent fetal dehydration is one suggestion.
These two hormones are secreted from the posterior pituitary gland. The roles of oxytocin in parturition and lactation are discussed in Chapters 21 (p. 416) and 36 (p. 657), respectively. Brown and colleagues (2013) have reviewed the complex mechanisms that promote quiescence of oxytocin systems during pregnancy. Levels of antidiuretic hormone, also called vasopressin, do not change during pregnancy.
hyrotropin-releasing hormone (TRH) is secreted by the hypothalamus and stimulates thyrotrope cells of the anterior pituitary to release thyroid-stimulating hormone (TSH), also called thyrotropin. TRH levels do not rise during normal pregnancy. However, TRH does cross the placenta and may serve to stimulate the fetal pituitary to secrete TSH (horpe-Beeston, 1991).