Steroid hormone receptors in the adrenal glands of fetal and adult rhesus monkeys.

TLDR: It is concluded that the lower concentration ofER in fetal adrenal glands is due to the absence of ER in the fetal zone, and the lack of ER and PR in the Fetal Zone suggests that estrogens and progestins do not influence the growth or function of the fetal Zone by receptor-mediated mechanisms.

Abstract: Sex steroid hormone receptors have been identified in the adrenal glands of rodents and may have a role in adrenal function. The highly estrogenic environment during pregnancy has been proposed to influence steroidogenesis by the fetal zone of the primate fetal adrenal gland. In order to determine whether these effects involve receptor-mediated mechanisms, we have examined the concentration and distribution of estrogen receptor (ER), androgen receptor, and progesterone receptor (PR) in the adrenal glands of fetal, immature, and adult rhesus monkeys. Monoclonal antibodies were used for immunocytochemistry (ICC), and in a gradient shift assay, for determination of receptor distribution and concentrations, respectively. There was no difference between the concentrations of ER in the adrenal glands from male and female adult animals (12.4 +/- 2.2, n = 3 and 13.2 +/- 2.0 fmol/mg DNA, n = 7; respectively); however, the concentration of ER in the fetal adrenal glands was markedly lower than in the adults (combined adult 12.7 +/- 1.6, n = 10, and fetal 0.9 +/- 0.4 fmol/mg DNA, n = 7; P less than 0.01). The concentration of ER in the adrenal glands of immature animals was also lower compared to adult animals (6.1 +/- 1.6, n = 6, P less than 0.05). In the adult, ICC revealed that staining for ER was restricted to the cell nucleus and was most dense in the zone fasciculata, with lesser staining in the zona glomerulosa and zona reticularis, and with no detectable staining in the medulla. ER staining was virtually absent in the fetal zone which comprises the major portion of the fetal gland; however, some staining was observed in the narrow definitive zone. The distribution of androgen receptor was similar to that of ER, whereas there was no detectable staining for PR in the adrenals of either adult or fetal animals. We conclude: 1) that the lower concentration of ER in fetal adrenal glands is due to the absence of ER in the fetal zone; 2) the lack of ER and PR in the fetal zone suggests that estrogens and progestins do not influence the growth or function of the fetal zone by receptor-mediated mechanisms; 3) estrogens and androgens may influence the function of the adult adrenal cortex.