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.
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Ludens, J.H., Vaughn, D.A. & Fanestil, D.D. Stimulation of urinary acidification by aldosterone and inhibitors of RNA and protein synthesis. J. Membrain Biol. 40 (Suppl 1), 199–211 (1978). https://doi.org/10.1007/BF02026006
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DOI: https://doi.org/10.1007/BF02026006