Stimulation of urinary acidification by aldosterone and inhibitors of RNA and protein synthesis

Summary

Urinary acidification by the urinary bladder of the toad (Bufo marinus) was stimulated, relative to control, by thein vitro addition of aldosterone (10⁻⁷ m), actinomycin D (20 μg/ml), puromycin (80 μg/ml) or cycloheximide (5 μg/ml). The action of the inhibitors of RNA or protein synthesis was not additive with that of aldosterone. This is opposite to the situation with Na⁺ transport, where the stimulation by aldosterone is abolished by the same concentrations of these inhibitors. That all agents enhanced urinary acidification was verified by: (i) measurement of RSCC (reverse short-circuit current) in the absence of Na⁺ transport, (ii) inhibition of RSCC by acetazolamide, an inhibitor of carbonic anhydrase, and (iii) direct measurement of the pH change of the mucosal (urinary) fluid. As in the case of Na⁺ transport, spirolactone inhibited the action of aldosterone. Although not a unique model, the apparent paradoxical mimicry of aldosterone's stimulation of urinary acidification may be explained by a model which includes action of aldosterone and the inhibitors via their known effects on RNA and protein synthesis.