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The K+ permeability of the apical membrane of frog skin (Rana temporaria) was analysed by recording the short-circuit current and its fluctuations in the presence of a mucosa-to-serosa-oriented K+ concentration gradient. Loading of the animals with KCl resulted in an augmentation of the Ba2+-blockade component of the short-circuit current and the plateau value of the K+-dependent relaxation noise. Poisoning of active transport and exposing both sides of the epithelium to KCl Ringer solution caused an increase of the K+ current and its fluctuations recorded after restoring the inward-oriented K+ gradient. Serosal quinidine (5 X 10(-4) M), which is thought to increase intracellular Ca2+ activity, depressed the K+ current and the relaxation noise. This effect was completely reversible. Removal of Na+ from the serosal solution, which is known to result in an elevation of intracellular Ca2+ by abolishing the driving force for the Na+/Ca2+ exchanger, also reduced the K+ current and the Lorentzian plateau. Both parameters returned to their control values after restoring the Na+ gradient across the basolateral membranes. It is concluded from these experiments that the apical K+ permeability is controlled by factors which depend on the intracellular K+ and Ca2+ concentration and that the apical K+ channels may constitute a pathway for K+ secretion.

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