Am J Physiol 1994 Jan 01;2661 Pt 2:F108-16. doi: 10.1152/ajprenal.1994.266.1.F108.

Effects of corticoid agonists and antagonists on apical Na+ permeability of toad urinary bladder.

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Effects of RU-28362 (glucocorticoid agonist), RU-38486 (glucocorticoid antagonist), and RU-26752 (mineralocorticoid antagonist) on the apical Na+ permeability of toad bladder were measured and correlated with occupancies of cytosolic type I (mineralocorticoid) and type II (glucocorticoid) receptors. Effects of the above steroids were measured in whole bladders, plasma membrane vesicles, and RNA-injected Xenopus oocytes. RU-38486 was found to fully displace aldosterone from type II receptors without affecting type I occupancy. Under these conditions, RU-38486 inhibited approximately 35% of the effect of aldosterone measured in the whole tissue and isolated membranes. Unexpectedly, oocytes injected with RNA from tissue stimulated with aldosterone plus RU-38486 expressed channel activity that was much higher than the sum of activities induced by either steroid alone. RU-28362 and RU-26752 at concentrations sufficient to fully occupy both receptors had only partial agonistic and antagonistic effects, respectively. The results suggest that at least one-third of the natriferic action of aldosterone measured in the amphibian urinary bladder is mediated by the glucocorticoid receptor. However, some of the effects observed cannot be accounted for by a simple receptor occupancy-response scheme.

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