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A Premature Increase in Circulating Cortisol Suppresses Expression of 11ß Hydroxysteroid Dehydrogenase Type 2 Messenger Ribonucleic Acid in the Adrenal of the Fetal Sheep¹

^a Department of Physiology, The University of Adelaide, Adelaide, South Australia 5000, Australia

We have investigated the effect of intrafetal cortisol administration, before the normal prepartum cortisol surge, on the expression of 11ß hydroxysteroid dehydrogenase (11ßHSD) type 2 mRNA in the fetal adrenal. We also determined whether increased fetal cortisol concentrations can stimulate growth of the fetal adrenal gland or increase expression of adrenal steroidogenic enzymes. Cortisol (hydrocortisone succinate: 2.0–3.0 mg in 4.4 ml/24 h) was infused into fetal sheep between 109 and 116 days of gestation (cortisol infused; n = 12), and saline was administered to control fetuses (saline infused; n = 13) at the same age. There was no effect of cortisol infusion on the fetal adrenal:body weight ratio (cortisol: 101.7 ± 5.3 mg/kg; saline: 108.2 ± 4.3 mg/kg). The ratio of adrenal 11ßHSD-2 mRNA to 18S rRNA expression was significantly lower, however, in the cortisol-infused group (0.75 ± 0.02) compared with the group receiving saline (1.65 ± 0.14). There was no significant effect of intrafetal cortisol on the relative abundance of adrenal CYP11A1, CYP17, CYP21A1, and 3ßHSD mRNA. A premature elevation in fetal cortisol therefore resulted in a suppression of adrenal 11ßHSD-2. Increased intra-adrenal exposure to cortisol at this stage of gestation is, however, not sufficient to promote adrenal growth or steroidogenic enzyme gene expression.

First decision: 7 October 1999.

¹ We acknowledge financial support from the National Heart Foundation of Australia and the Australian Research Council.

² Correspondence: I.C. McMillen, Department of Physiology, The University of Adelaide, Fourth Floor North Wing, Medical School Building, Frome Road, Adelaide, SA 5000, Australia. FAX: 08 8303 3356; caroline.mcmillen{at}adelaide.edu.au

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