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Development of the Baboon Fetal Adrenal Gland: Regulation of the Ontogenesis of the Definitive and Transitional Zones by Adrenocorticotropin¹

Department of Physiological Sciences, Eastern Virginia Medical School (M.G.L., G.J.P.), Norfolk, Virginia 23501; and the Departments of Obstetrics/Gynecology/Reproductive Sciences and Physiology, Center for Studies in Reproduction, University of Maryland School of Medicine (E.D.A.), Baltimore, Maryland 21201

Address all correspondence and requests for reprints to: Gerald J. Pepe, Ph.D., Department of Physiological Sciences, Eastern Virginia Medical School, P.O. Box 1980, Norfolk, Virginia 23501-1980. E-mail: gjp{at}borg.evms.edu

Throughout gestation, the primate fetal adrenal gland is comprised of the fetal zone, which expresses the P-450 17-hydroxylase-C17,20 lyase (P-450c17) enzyme that catalyzes the synthesis of C₁₉ steroids used for placental estrogen production. The development of the transitional zone comprised of cortical cells that express the P-450c17 and the 3ß-hydroxysteroid dehydrogenase-isomerase (3ßHSD) enzymes for cortisol production, and the definitive zone, which expresses 3ßHSD, but not P-450c17, for mineralocorticoid synthesis, does not occur until relatively late in gestation. Although ACTH is considered essential to fetal adrenal growth and function, the role that ACTH has in the development of the transitional and definitive zones, is less clear. To answer this question, the width of these zones was determined by immunocytochemical expression of P-450c17 and/or 3ßHSD in fetal adrenal glands obtained on day 100 (mid) of gestation (term = day 184) from baboons in which ACTH was administered to the fetus on days 95–99 of gestation or on day 165 (late) of gestation from baboons in which fetal ACTH was suppressed by treatment of the mother and fetus with betamethasone on days 150–164 of gestation. At midgestation, the fetal adrenal was comprised almost exclusively of fetal zone cells and a small definitive zone (38 ± 2 µm in width), but was essentially devoid of a transitional zone (7 ± 2 µm). Treatment with ACTH enhanced (P < 0.05) the width of the transitional zone (67 ± 4 µm), but not the size of the definitive zone (10 ± 4 µm). In late gestation, the width of the definitive zone, although 2-fold greater than that on day 100, was smaller (P < 0.05) than that of the transitional zone (120 ± 15 µm), which greatly exceeded that at midgestation. Treatment with betamethasone in late gestation eliminated the transitional zone, but had no effect on the size of the definitive zone (120 ± 8 µm). These findings indicate that the development of the baboon fetal adrenal transitional zone late in gestation is dependent on fetal pituitary ACTH. In contrast, the ontogenesis of the definitive zone at midgestation and its growth in late gestation occur in the relative absence of ACTH.

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