G. Hirasawa et al., 11 beta-hydroxysteroid dehydrogenase type 2 and mineralocorticoid receptorin human fetal development, J CLIN END, 84(4), 1999, pp. 1453-1458
11 beta-Hydroxysteroid dehydrogenase type II (11 beta HSD2) confers specifi
city on the mineralocorticoid receptor (MR) by converting biologically acti
ve glucocorticoids to inactive 11-keto metabolites. The biological signific
ance of 11 beta HSD2 activity during fetal development is currently being e
xplored, but the temporal and spatial distributions of the enzyme and recep
tor have not been examined. We therefore examined their distributions durin
g Various stages of human fetal development using immunohistochemistry. Bat
h 11 beta HSD2 and MR immunoreactivity were detected in the distal convolut
ed and collecting tubules of the kidney from early in gestation. Fetal skin
, intermediate layer of the epidermis, peridermal cells, and hair follicles
were positive for both 11 beta HSD2 and MR. Weak 11 beta HSD2 and MR immun
oreactivity was detected in the superficial ciliated epithelium of the esop
hagus, the deep layer of gastric epithelial cells, and the superficial epit
helium of the small intestine. Columnar epithelium in the terminal bronchio
lar budding component of fetal lung and tracheal and bronchial ciliated epi
thelium were also positive for MR and 11 beta HSD2 from early gestation. Co
lonic epithelium and pancreatic exocrine duct cells, which demonstrated mar
ked immunoreactivity of both MR and 11 beta HSD2 in the adult, did not expr
ess MR and 11 beta HSD2 until very late in gestation. These results imply t
hat mineralocorticoid action in the upper fetal gastrointestinal tract, kid
ney, shin, and lung is facilitated by 11 beta HSD2 and is involved in water
and electrolyte transport between fetus and amniotic fluid as well as feta
l urine production.