Corticosteroid dynamics in the nonpregnant, pregnant, and postpartum spontaneously hypertensive rat

Factors responsible for hypertension in the spontaneously hypertensive rat (SHR) remain under investigation. As in human pregnancy complicated by essential chronic hypertension, the hypertension of the pregnant SHR subsides and returns postpartum. Because corticosteroid excess can cause hypertension, we examined several aspects of adrenocortical activity as potentially affecting the reported blood pressure profiles of nonpregnant, term pregnant, and postpartum SHR, using normotensive Wistar-Kyoto (WKY) rats as controls. We found that corticosterone levels were comparable in nonpregnant SHR and WKY rats, and unaffected by pregnancy. No differences were detected postpartum. Although pregnancy was accompanied by significant increases in plasma aldosterone levels, no interbreed differences were observed, which remained the case postpartum. Single adrenal cell secretion of aldosterone and corticosterone, as detected by reverse hemolytic plaque assay, yielded similar results in the pregnant and postpartum rat. Hormone responses to dietary manipulations in the nonpregnant and pregnant SHR and WKY suggest an important role for ACTH, and a lesser one for AII in the regulation of corticosteroids. In situ hybridization histochemistry, using a probe that detects both P450c11beta and P450c11AS mRNA, revealed comparable message density and zonal distribution in adrenals from pregnant and nonpregnant SHR and WKY rats. Breed- and pregnancy-dependent differences in adrenal expression of P450scc, P450c11beta, and P450c11AS were noted. In summary, our findings suggest that although some discrepancies exist in the aspects of adrenocortical activity examined, they are unlikely to be etiologic in the blood pressure profile observed in nonpregnant, pregnant, and postpartum SHR.