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Corticotropin-Releasing Hormone Type I Receptor Messenger Ribonucleic Acid and Protein Levels in the Ovine Fetal Pituitary: Ontogeny and Effect of Chronic Cortisol Administration¹

Departments of Physiology and Pharmacology (J.L.G., J.P.F., J.S., J.C.R.) and Obstetrics and Gynecology (J.P.F, G.A.M., J.S., J.C.R.) and Perinatal Research Laboratory (J.L.G., J.P.F., G.A.M., J.S., J.C.R.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1066

Address all correspondence and requests for reprints to: Dr. James C. Rose, Department of Obstetrics and Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157. E-mail: jimrose{at}wfubmc.edu

In sheep, the ACTH secretory response to CRH in vivo or in vitro changes as a function of development, with peak responses occurring several weeks before term (145 days of gestation). CRH-stimulated ACTH secretion is mediated via the G protein-coupled CRH type I (CRH R1) receptor. We used a quantitative ribonuclease protection assay and Western immunoblotting to determine messenger RNA (mRNA) and protein levels of the CRH R1 receptor in immature and mature fetuses and adults. In addition, we precociously elevated fetal plasma cortisol levels to determine whether the fetal CRH R1 receptor is sensitive to increases in plasma cortisol.

CRH R1 receptor mRNA levels decreased markedly throughout gestation and into the transition to adult life (immature fetus, 1.24 ± 0.17; mature fetus, 0.75 ± 0.13; adult, 0.18 ± 0.093 pg/µg total anterior pituitary RNA). Also, continuous cortisol infusion in immature fetuses significantly decreased CRH R1 mRNA levels by 41%. Similar decreases were noted in protein levels. Thus, the decreased ACTH response to CRH stimulation during late gestation may be related to decreased CRH R1 receptor expression. In addition, plasma cortisol levels may influence corticotroph responsiveness to CRH by decreasing CRH R1 receptor expression.

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