THE EFFECT OF CHLORMERODRIN ON THE ISOLATED TOAD BLADDER

¹ Departments of Physiology and Pharmacology, University of Kansas Medical Center, Kansas City, Kansas

Administration of chlormerodrin to the serosal surface of the isolated toad bladder promptly reduced the transbladder potential difference, reduced short-circuit current (SCC) after a 20-min latent period and increased tissue conductance. Mucosal application had no effect. The two unidirectional Na fluxes across the bladder were measured with Na²³ in separate experiments. Chlormerodrin depressed the mucosa to serosa flux in the first 30-min period but did not affect the average SCC. In the second 30-min period both mucosa to serosa flux and SCC were depressed, but the latter fell to a much greater extent. In another series of experiments, chiormerodrin also increased the passive Na flux from serosa to mucosa in the second 30-min drug period. We conclude that chiormerodrin inhibits net Na transport in this tissue by depressing the mucosa to serosa flux, possibly by a direct effect on an active transport mechanism and by increasing the passive serosa to mucosa flux through an effect on tissue permeability. The receptors for mercurials in the toad bladder are dissimilar to those in the kidney. The nondiuretic mercurial, p-chloromercuribenzoate, also inhibited the SCC. Cysteine blocked the effect of chlormerodrin, and dimercaprol did not reverse it.