There is increasing evidence that the intrauterine milieu and corticosteroi
d exposure play a role in the etiology of hypertension. We examined adrenoc
ortical gene expression and circulating corticosteroids in the d 21 fetal s
pontaneously hypertensive rat (SHR) and its normotensive genetic control, t
he Wistar-Kyoto (WKY) rat. By RNase protection assays, we found no differen
ces in the relative abundances of mRNAs for P450scc and P450c11 beta, and b
arely detectable P450c11AS mRNA in the adrenals of fetal SHR and WKY rats.
P450c11B3 RNA was undetectable by reverse transcription polymerase chain re
action in both SHR and WKY fetuses. The zonal expression of P450c11 mRNA wa
s comparable in SHR and WKY fetuses by in situ hybridization histochemistry
. There were no significant differences in peripheral levels of aldosterone
and corticosterone by radioimmunoassay in fetal SHR and WKY rats. Based up
on the absence of distinct differences in the aspects of adrenocortical act
ivity examined, it is unlikely that they are integral in the programming of
hypertension in this model.