McCall A L, Stern J, Dale S L, Melby J C
Endocrinology. 1978 Jul;103(1):1-5. doi: 10.1210/endo-103-1-1.
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.
对通过给予甲基雄烯二醇(MAD;17α-甲基-5-雄烯-3β,17β-二醇)而患高血压的大鼠以及对照大鼠在治疗期间定期进行肾上腺静脉插管。所有接受MAD治疗的大鼠在7周时均患高血压。在接受MAD治疗的大鼠中,皮质酮的分泌在所有时间均持续下降。与对照组相比,在第2、4和6周时,18-羟基-11-脱氧皮质酮分泌减少,而11-脱氧皮质酮(DOC)分泌增加。在第2和4周时醛固酮分泌减少。本研究显示了肾上腺11-羟化和18-羟化的体内阻滞。通过MAD治疗导致的短暂DOC蓄积产生了高血压,尽管在高血压形成时DOC分泌过多以及类固醇生成的其他变化正在减弱。