Abstract

Responses of apical and basolateral membrane conductances after stimulation with dexamethasone for 24 h were analyzed in differentiated cultured renal tight epithelia (A6). Specific membrane conductances were assessed with microelectrodes and standard equivalent circuit analysis. Apical membrane conductance (ga), which was linearly related with spontaneous variations in short-circuit current (Isc) of control tissues, increased significantly after dexamethasone. The relationship between ga and Isc of the combined data from control and stimulated tissues conforms with a function of the second degree. The nonlinearity originates essentially from a decrease in the electrochemical driving force for Na+ entry at higher levels of ga. Basolateral border conductance (gb) increased after dexamethasone, but was not related with Isc under either condition. The increase in gb, which was not due to partial K+ conductance, appears to reflect nonspecific effects after dexamethasone. It was missing when elevation of Na+ entry after dexamethasone was prevented by simultaneous addition of apical amiloride in low concentrations. The data demonstrate that apical membrane Na+ channels are the target for dexamethasone.

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