Chloride conductance of frog skin: localization to the tight junctions?

The pathway(s) of passive conductive Cl transport across isolated frog skin are analyzed by electrophysiological techniques including microelectrode impalement of principal cells. It is found that the apical membrane of granular cells is virtually impermeable for Cl. Substitution of mucosal Cl by anions except NO3 and SCN decreases Cl-related tissue conductance (gCl) with first order kinetics. NO3 and SCN block gCl with half-maximal concentration of 18 and 5 mM, respectively. Omission of serosal Cl has little effect on gCl unless the inhibiting anions NO3 or SCN are used. The putative Cl channel blocker diphenylaminocarbonic acid (DPC) and some analogs inhibit gCl, half-inhibitory concentration of the most potent dichloro-DPC is 10(-6) M. The inhibitors act only from the mucosal side. Slow dissipation of gCl after abolition of Na entry across the apical membranes which can be prevented by preceding blockage of the Na-K-ATPase with ouabain suggests that the intracellular Na activity might influence the permeability of the Cl pathway. It is supposed that this control involves microfilaments between the cytoskeleton and the tight junctions with Cl-specific permeation sites in outer regions of the junctional complex.