Functional capacity of fetal zone cells of the baboon fetal adrenal gland:A major source of alpha-inhibin

We have shown that ACTH receptor mRNA expression and steroidogenesis were i ncreased in the transitional zone and decreased in the fetal zone of the ba boon fetal adrenal in the second half of gestation. Thus, we proposed that there is a divergence in ACTH receptor-mediated zone-specific steroidogenes is within the fetal adrenal during mid to late gestation. We have also demo nstrated that fetal serum alpha-inhibin levels decline with advancing devel opment. It is possible, therefore, that the alpha subunit of inhibin provid es a good marker of fetal zone cellular function and that the changes in ci rculating fetal alpha-inhibin with advancing pregnancy reflect ontogenetic changes in fetal adrenal cortical zone-specific cell function. However, if remains to be determined whether the fetal adrenal is a major source of cir culating alpha-inhibin in the fetus and whether alpha-inhibin expressed in the fetal, definitive, and/or transitional zones. Therefore, the current st udy compared fetal serum alpha-inhibin levels with immunocytochemical local ization of alpha-inhibin in baboon fetal adrenals obtained on Days 60 (earl y), 100 (mid), and 165 or 182 (late) of gestation (term averages Day 184) f rom animals untreated or treated with betamethasone, which we previously de monstrated suppressed fetal pituitary ACTH and adrenal weight. Fetal serum alpha-inhibin levels (mean +/- SE) were greater (p < 0.05) at mid (5863 +/- 730 mu l eq/ml) than at late (3246 +/- 379) gestation and were reduced (p < 0.05) by betamethasone. The inhibin alpha subunit was expressed in abunda nt quantities in the fetal adrenal cortex, but not in medulla, throughout g estation. Air mid and late gestation, alpha-inhibin was expressed throughou t the fetal adrenal cortex but most intensely in the innermost area of feta l zone cells. By late gestation, the fetal adrenal exhibited a gradient of alpha-inhibin expression. Thus, the outermost definitive zone cells were de void of alpha-inhibin, the transitional zone exhibited a relatively low alp ha-inhibin content, and fetal zone cells continued to exhibit extensive exp ression of alpha-inhibin. Betamethasone diminished the intensity of alpha-i nhibin expression throughout the fetal adrenal cortex. These results indica te that the fetal adrenal fetal zone is a significant source of circulating alpha-inhibin in the baboon fetus and that alpha-inhibin provides a good m arker to study the developmental regulation of fetal zone-specific adrenoco rtical function.