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Am J Physiol Cell Physiol 264: C317-C322, 1993;
0363-6143/93 $5.00
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AJP - Cell Physiology, Vol 264, Issue 2 C317-C322, Copyright © 1993 by American Physiological Society

ARTICLES

Corticosterone induces 11 beta-HSD and mineralocorticoid specificity in an amphibian urinary bladder cell line

H. P. Gaeggeler, H. Duperrex, S. Hautier and B. C. Rossier
Institut de Pharmacologie et de Toxicologie de l'Universite, Lausanne, Switzerland.

We have examined the mineralocorticoid specificity in a TBM 18-23 cell line derived from the toad bladder epithelium. In cells grown on porous substrate, corticosterone was more potent than aldosterone in stimulating a sodium transport response, measured by the short-circuit current method 6 h after hormone addition [mean affinity constant (K0.5) for corticosterone = 1 nM vs. K0.5 for aldosterone = 8 nM]. The time course of effects and saturation kinetics were identical for both agonists, suggesting interaction with identical receptors. Whereas the dose-response relationship for aldosterone did not change with time of incubation (6 vs. 24 h), the dose-response curve for corticosterone became biphasic at 24-h incubation (apparent K0.5 as high as 40 nM), demonstrating that corticosterone became apparently less potent with time. Pretreatment with carbenoxolone, a potent inhibitor of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), restored full sensitivity at 24-h incubation to corticosterone. The 11 beta-HSD activity was low during the first 3 h of incubation in the presence of 3 nM corticosterone, and only a small fraction (approximately 7%) of corticosterone was metabolized. At 24-h incubation, 11 beta-HSD activity increased approximately 2.5-fold (P < 0.001, n = 8). We conclude that 11 beta-HSD activity is induced by its own substrate in TBM cells in parallel with the induction of the carbenoxolone-sensitive sodium transport response.


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[Abstract] [Full Text]


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