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The intracellular sodium ion activity (aiNa), apical membrane potential (psi ac) and apical sodium electrochemical driving force (delta mu Na) in Rana temporaria skin were measured using double-barrelled sodium-sensitive micro-electrodes, in the presence of various apical sodium activities (aoNa), amiloride, ouabain, and during voltage clamp of psi ac. The permeability and specific conductance of the apical cell membrane to sodium entry (PaNa and GaNa respectively) were calculated from the Goldman-Hodgkin-Katz equation and the Nernst-Planck (electrodiffusion) permeability equations respectively. The roles of aoNa and aiNa in the control of apical sodium entry were studied. PaNa increased linearly with log decrease in aoNa between 79 and 0.01 mM. Under short-circuit conditions, aiNa remained constant over the aoNa range of 10-79 mM, but decreased when aoNa was lower than 10 mM, due to a fall in delta mu Na and GaNa. Amiloride decreased PaNa, GaNa and aiNa, a result analogous to that observed in spontaneous low-transporting skins. Ouabain inhibited sodium transport and increased aiNa before any changes in PaNa occurred. The latter decreased only when aiNa rose above 15 mM. Increasing delta mu Na by hyperpolarizing voltage clamp of the apical cell membrane elicited a saturable increase in aiNa. The opposite effect was elicited by depolarizing psi ac. Electrodiffusion appears to be the sole mode of apical sodium entry.

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