There is increasing evidence that the intrauterine milieu and corticosteroid exposure play a role in the etiology of hypertension. We examined adrenocortical gene expression and circulating corticosteroids in the d 21 fetal spontaneously hypertensive rat (SHR) and its normotensive genetic control, the Wistar-Kyoto (WKY) rat. By RNase protection assays, we found no differences in the relative abundances of mRNAs for P450scc and P450c11&bgr;, and barely detectable P450c11AS mRNA in the adrenals of fetal SHR and WKY rats. P450c11B3 RNA was undetectable by reverse transcription polymerase chain reaction in both SHR and WKY fetuses. The zonal expression of P450c11 mRNA was comparable in SHR and WKY fetuses byin situhybridization histochemistry. There were no significant differences in peripheral levels of aldosterone and corticosterone by radioimmunoassay in fetal SHR and WKY rats. Based upon the absence of distinct differences in the aspects of adrenocortical activity examined, it is unlikely that they are integral in the programming of hypertension in this model.