Abstract

(1) Combined use of external Cl concentration pulses and apical membrane depolarization permitted to compare the roles of apical voltage and Cl ions upon the activation of a skin Cl conductance, GCl, which is assumed to reflect activation of the permeability of a Cl pathway. (2) Apical membrane depolarization induced by skin hyperpolarization, or by short-circuiting skins with high K Ringer's on the inner side, failed to activate GCl in the absence of external Cl, GCl remaining negligible. Under apical membrane depolarization, a step elevation of [Cl]0 slowly activated GCl as characterized by a sigmoidal current response of slow onset concomitant to a slow conductance increase. External Cl removal had the reverse effect, slowly inactivating GCl. (3) With the apical membrane in the normal polarized state, a step increase of [Cl]0 slowly activated GCl to submaximal values. This indicates that the interaction of Cl ions with the apical membrane partially activates GCl in the absence of apical membrane depolarization. (4) Activation of GCl was interpreted on the basis of a direct effect of Cl ions upon the apical membrane, having been attributed to the apical membrane voltage an indirect role. Voltage would affect the Cl distribution across the apical membrane, and, as a result, the Cl concentration at a proposed regulatory site which modulates the apical membrane permeability to Cl ions.

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