Adrenal Steroidogenesis in Methylandrostenediol-Induced Hypertension*

Abstract
Adrenal vein catheterizations were done in rats made hypertensive by administration of methylandrostenediol (MAD; 17.alpha.-methyl-5-androstene-3.beta.,-17.beta.-diol), and in control rats at intervals during treatment. All MAD-treated rats were hypertensive by 7 wk. Secretion of corticosterone was consistently decreased at all times in MAD-treated rats. 18-Hydroxy-11-deoxycorticosterone secretion and 11-deoxycorticosterone (DOC) secretion decreased and increased, respectively, compared to controls at 2, 4 and 6 wk. Aldosterone secretion was decreased at 2 and 4 wk. This study shows an in vivo block of adrenal 11- and 18-hydroxylation. Transient DOC accumulation by treatment with MAD produced hypertension, though DOC oversecretion and other changes in steroidogenesis were waning by the time hypertension developed.