help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schane, H. P.
Right arrow Articles by Snyder, B. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schane, H. P.
Right arrow Articles by Snyder, B. W.

Endocrinology, Vol 114, 1983-1989, Copyright © 1984 by Endocrine Society

ARTICLES

Nivazol: a glucocorticoid in rats with only hypothalamic-pituitary- adrenal-inhibiting activity in primates

HP Schane, HR Harding, JE Creange, I Botton, VD Castracane and BW Snyder

The synthetic steroid nivazol lacks three of the substituents considered to be important for glucocorticoid activity, i.e. the 3- keto, the 11-hydroxy, and the 20-keto groups. Nevertheless, in the rat, nivazol has the activity profile of a glucocorticoid. After treatment of intact female rats with nivazol , the mean weights of the adrenals and thymus were lower than those in the vehicle-treated control group. The results were qualitatively and quantitatively similar to those obtained with methylprednisolone. Thymolysis as well as liver glycogen deposition were seen in adrenalectomized rats treated with nivazol , and eosinopenia and inhibition of carrageenan edema were noted in intact rats. In the rhesus monkey, treatment with nivazol resulted in a marked reduction in circulating cortisol levels and elimination of the diurnal pattern, although a dose 10 times that needed to reduce circulating cortisol levels did not produce eosinopenia or increase fasting blood glucose levels. Both eosinopenia and higher fasting blood glucose levels were seen after treatment with methylprednisolone. Nivazol did not prevent the ACTH-induced increase in circulating cortisol levels nor did it alter circulating aldosterone levels. Therefore, suppression of ACTH is the predominant if not the sole action of nivazol in the primate. Preliminary results in clinical trials suggest a similar activity profile in humans. Therefore, nivazol elicits numerous glucocorticoid activities in the rodent, but only the inhibition of the hypothalamic-pituitary-adrenal axis was observed in the primate. It is of special interest that the inhibition of the hypothalamic-pituitary-adrenal axis occurs without altering circulating aldosterone levels and without evidence of debilitating catabolic activity.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1984 by The Endocrine Society