During pregnancy maternal plasma corticotrophin-releasing hormone (CRH
) levels rise 1000-fold whilst fetal plasma levels are often 100-fold
higher than the concentrations seen in normal non-pregnant human plasm
a. Despite these high CRH levels neither the maternal nor fetal pituit
ary releases excessive amounts of ACTH. A specific CRH-binding protein
(CRHBP) exists in the maternal circulation which is able to bind and
inactivate the ACTH releasing activity of CRH. In this study we have u
sed a specific CRHBP radioimmunoassay to determine the level of CRHBP
in fetal and maternal plasma samples. Fetal samples were collected by
cordocentesis between 20 and 33 weeks gestation and matched maternal s
amples were taken by venepuncture at the same time. In a second study,
plasma samples were collected h-om 8 women at fortnightly intervals f
rom week 20 to term, at labour and post-partum A fetal sample, taken f
rom the umbilical vein, was collected immediately post-delivery. The m
ean maternal CRHBP concentration for the samples collected between 20
and 33 weeks (n=23) was 8.12 nmol/l and the fetal level was 8.62 nmol/
l. Data from the second study showed that at term the maternal CRHBP c
oncentration decreased significantly (P<0.025) to 6.32 nmol/l. The fet
al CRHBP level also decreased significantly (P<0.001) at term to a lev
el of 5.84 nmol/l. The CRHBP in both fetal and maternal plasma was sho
wn to be functional by I-125-CRH binding and gel permeation chromatogr
aphy. The capacity of maternal and fetal plasma to bind I-125-CRH decr
eased at term in agreement with the quantitation of plasma CRHBP by ra
dioimmunoassay.