Regulates transfer of calcium and other solutes; regulates fetal mineral homeostasis nizing hormone; TSH = thyroid-stimulating hormone.
amnionic fluid declines, and near term the levels are approximately 20 percent of those in maternal plasma.
Maternal urine contains the same variety of hCG degradation products as maternal plasma. The principal urinary form is the terminal product of hCG degradation, namely, the 500 400 300�I 0E , 200£:) 100 , ..--, , , ,
I I 4, , I :t > II II ,, 3.1 c 40 I \ , , c
I \, " , , 2
FIGURE 5-18 Distinct profiles for the concentrations of human chorionic gonadotropin (hCG), human placental lactogen (hPL), and corticotropin-releasing hormone (CRH) in serum of women throughout normal pregnancy.
�-core fragment. Concentrations of this fragment follow the same general pattern as that in maternal plasma, peaking at approximately 10 weeks' gestation. Importantly, the so-called �-subunit antibody used in most pregnancy tests reacts with both intact hCG-the major form in the plasma, and with fragments of hCG-the major forms found in urine.
Placental gonadotropin-releasing hormone (GnRH) is likely involved in the regulation of hCG formation. Both GnRH and its receptor are expressed by cytotrophoblasts and by the syncytiotrophoblast (Wolfahrt, 1998). GnRH administration elevates circulating hCG levels, and cultured trophoblasts respond to GnRH treatment and raise hCG secretion (Iwashita, 1993; Siler-Khodr, 1981). Pituitary GnRH production also is regulated by inhibin and activin. In cultured placental cells, activin stimulates and inhibin inhibits GnRH and hCG production (Petraglia, 1989; Steele, 1993).
Renal clearance of hCG accounts for 30 percent of its metabolic clearance. he remainder is likely cleared by metabolism in the liver (Wehmann, 1980). Clearances of�-and .-subunits are approximately 10-and 30-fold, respectively, greater than that of intact hCG. In pregnancies complicated by chronic renal disease, hCG clearance can be markedly decreased.
Both hCG subunits are required for binding to the LH-hCG receptor in the corpus lute un and the fetal testis. LH-hCG receptors are present in various other tissues, but their roles there are less defined.
he best-known biological function of hCG is the so-called rescue and maintenance of corpus luteum function-that is, continued progesterone production. This is only an incomplete explanation for the physiological function of hCG in pregnancy. For example, maximum plasma hCG concentrations are attained well after hCG-stimulated corpus luteum secretion of progesterone has ceased. Speciically, luteal progesterone synthesis begins to decline at about 6 weeks despite continued and increasing hCG production.
A second hCG role is stimulation of fetal testicular testosterone secretion. This is maximum approximately when hCG levels peak. hus, at a critical time in male sexual diferentiation, hCG enters fetal plasma from the syncytiotrophoblast. In the fetus, it acts as an LH surrogate to stimulate Leydig cell replication and testosterone synthesis to promote male sexual differentiation (Chap. 3, p. 35). Before approximately 110 days, there is no vascularization of the fetal anterior pituitary from the hypothalamus. Thus, pituitary LH secretion is minimal, and hCG acts as LH before this time. hereafter, as hCG levels fall, pituitary LH maintains modest testicular stimulation.