Adrenal steroidogenesis in methylandrostenediol-induced hypertension.

Abstract

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.

• Authors: A L McCall, J Stern, S L Dale, J C Melby
• Journal: Endocrinology (Endocrinology) Vol. 103 Issue 1 Pg. 1-5 (Jul 1978) ISSN: 0013-7227 [Print] United States
• PMID: 744061 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• 18-Hydroxydesoxycorticosterone
• Steroids
• Methandriol
• Corticosterone
• Cortodoxone

Topics

• 18-Hydroxydesoxycorticosterone (metabolism)
• Adrenal Glands (physiopathology)
• Animals
• Blood Pressure
• Body Weight
• Corticosterone (metabolism)
• Cortodoxone (metabolism)
• Female
• Hypertension (chemically induced, physiopathology)
• Methandriol
• Rats
• Steroids (metabolism)