Regulation of placental growth and chorionic somatomammotropin in the rhesus monkey: effects of protein deprivation, fetal anencephaly, and placental vessel ligation.

An isocaloric protein-deficient diet (0.5 gm/kg of body weight) was administered throughout pregnancy to 10 rhesus monkeys (Macaca mulatta). Ligation of the fetal interplacental bridging vessels (n = 6) and functional fetal hypophysectomy (experimental induction of anencephaly) (n = 10) were performed at midgestation. Monkey chorionic somatomammotropin (mCS) concentrations were measured serially in maternal plasma and in fetal plasma at birth. Fetal weight, trimmed placental weight, and placental DNA content were determined near term in the experimental groups and in controls matched for gestational age. Maternal mCS concentrations rose steadily until term and this rise paralleled the increase in placental weight (mCS at term = 16.5 +/- 0.90 microgram/ml in maternal plasma and 0.024 +/- 0.001 microgram/ml in fetal plasma). At term, maternal mCS correlated with placental DNA (r = 0.61, P less than 0.01) and placental weight (r = 0.49, P less than 0.01), but not fetal weight. Maternal mCS levels were not affected by protein deprivation, fetal anencephaly, or ligation of the interplacental bridging vessels. Maternal protein deprivation had a negative effect on fetal birth weight (409 +/- 22 versus 472 +/- 18 gm for controls, P less than 0.05) and maternal weight gain during pregnancy but had no effect on placental DNA or trimmed placental weight. Fetal anencephaly resulted in a 23% reduction in trimmed placental weight, no change in placental DNA, a 40% reduction in fetal body weight, and a reduced fetal/placental weight ratio. Ligation of interplacental bridging vessels resulted in atrophy of the secondary placental disc, an increase in weight and DNA content of the primary placenta, and normal fetal weight. We have concluded that the hemochorial placenta of the rhesus monkey responds to interruption of the fetal villous circulation in the first half of gestation by initiating compensatory hyperplasia. Placental cellular replication in the second half of rhesus pregnancy in minimally regulated by the fetal central nervous system or the pituitary gland. Secretion of mCS is primarily controlled by the mass of functioning trophoblast.