Carbonic anhydrase (CA) facilitates acid-base transport in several tissues.
Acidosis upregulates membrane-bound SDS-resistant hydratase activity in va
rious tissues and CA IV mRNA in rabbit kidney. This study was designed to a
ssess whether the expression of membrane-bound CA IV isozyme in mouse place
nta is regulated developmentally and by maternal ammonium chloride loading
at the end of pregnancy. For this purpose we used Northern blot analysis, W
estern blots of microsomal membranes, and immunocytochemistry. The expressi
on of CA IV mRNA on Northern blots tripled from day 11 to day 15 and then r
emained stable until the end of pregnancy. Expression of CA IV immunoreacti
ve protein on Western blot tripled from day 11 to day 15 and decreased almo
st to baseline by day 19. Strong staining for CA IV was detected by immunoc
ytochemistry in labyrinthine trophoblast, in the endodermal layer of the yo
lk sac (both intra- and extraplacental) and in the uterine epithelium. Weak
staining was observed in most fetal endothelial cells at 11 days but not l
ater in gestation. Maternal acidosis did not upregulate the expression of C
A IV mRNA or CA IV immunoreactive protein. Thus CA IV expression in mouse p
lacenta is developmentally regulated. Maternal acidosis during the last qua
rter of pregnancy does not upregulate CA IV mRNA or CA IV immunoreactive pr
otein.