Abstract
In the rat, the conformationally highly bent steroid 21-hydroxy-6,19-oxidoprogesterone efficiently displaces [3H]corticosterone from thymus-glucocorticoid receptors and blocks type II receptors in kidney cytosols but competes with neither [3H]aldosterone for kidney-mineralocorticoid receptors nor [3H]progesterone for uterus-progesterone receptors. It evokes Na+ retention only at very high doses (∼100 μg/100 g of rat weight) and is unable to induce tyrosine aminotransferase or to increase glycogen deposits in rat liver. When coincubated with corticosterone or dexamethasone, 2.5 μm21OH-6OP inhibits 80% of tyrosine aminotransferase induction. It may therefore be used experimentally as an antiglucocorticoid virtually lacking mineralocorticoid or glucocorticoid properties as well as affinity for mineralocorticoid or progesterone receptors.
Footnotes
- Received February 18, 1997.
- Accepted April 24, 1997.
-
Send reprint requests to: Dr. G. P. Vicent, Departamento de Quı́mica Biológica, Ciudad Universitaria, Pabellón 2.–1428 Buenos Aires, Argentina. E-mail:gvicent{at}qb.fcen.uba.ar
-
↵1 Current affiliation: Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, MI 48109-0632
- The American Society for Pharmacology and Experimental Therapeutics
MolPharm articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|