Adrenal steroidogenesis in methylandrostenediol-induced hypertension.
Adrenal vein catheterizations were done in rats made hypertensive by administration of methylandrostenediol (MAD; 17alpha-methyl-5-androstene-3beta,-17beta-diol), and in control rats at intervals during treatment. All MAD-treated rats were hypertensive by 7 weeks. 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 weeks. Aldosterone secretion was decreased at 2 and 4 weeks. 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.
D015070:18-Hydroxydesoxycorticosterone / Q000378:metabolism; D000311:Adrenal Glands / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D003345:Corticosterone / Q000378:metabolism; D003350:Cortodoxone / Q000378:metabolism; D005260:Female; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008695:Methandriol; D051381:Rats; D013256:Steroids / Q000378:metabolism*
D015070:18-Hydroxydesoxycorticosterone; D013256:Steroids; D008695:Methandriol; D003345:Corticosterone; D003350:Cortodoxone