In humans, the length of gestation and the onset of parturition have been l
inked to the exponential production of placental CRH and a late gestational
decline in maternal plasma CRH-binding protein (CRH-BP). CRH has been show
n to have direct effects on the myometrium and on the fetal adrenal, where
it stimulates production of the estrogen precursor dihydroepiandrosterone s
ulfate. In vitro placental CRH production is stimulated by cortisol and inh
ibited by progesterone. To determine whether this mechanism might operate i
n other apes, we sampled eight chimpanzees and two gorillas through their p
regnancies for CRH, CRH-BP, cortisol, estradiol, progesterone, and alpha-fe
toprotein. We show that both chimpanzee and gorilla maternal plasma CRH con
centrations rise exponentially as observed in the human. The gorillas exhib
ited a human-like antepartum fall in CRH-BP, whereas CRH-BP in the chimpanz
ee remained stable. Pregnancy-associated changes in cortisol, estradiol, pr
ogesterone, and alpha-fetoprotein were qualitatively similar to those obser
ved in humans. Maternal plasma cortisol correlated with plasma CRH in both
gorillas (r = 0.60; P < 0.05) and chimpanzees (r = 0.36; P < 0.02). Further
, there was a strong correlation between plasma estradiol and the log of pl
asma CRH in the gorilla (r = 0.93; P < 0.0001) and in the chimpanzee (r = 0
.72; P < 0.001), which is consistent with the hypothesis that placental CRH
determines the placental production of estradiol by stimulating the produc
tion of fetal adrenal dehydroepiandrosterone sulfate. Plasma CRH and proges
terone were positively correlated providing no in vivo support for progeste
rone inhibition of CRH release.