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Abstract

Cell membrane potentials of rat kidney proximal tubules were measured in response to peritubular ion substitutions in vivo with conventional and Cl⁻ sensitive microelectrodes in order to test possible alternative explanations of the bicarbonate dependent cell potential transients reported in the preceding paper. Significant direct effects of bicarbonate on peritubular K⁺, Na⁺, and Cl⁻ conductances could be largely excluded by blocking K⁺ permeability with Ba²⁺ and replacing all Na⁺ and Cl⁻ by choline or respectively SO₄²⁻ isethionate, or gluconate. Under those conditions the cell membrane response to HCO₃^- was essentially preserved. In addition it was observed that peritubular Cl⁻ conductance is negligibly small, that Cl⁻/HCO₃^- exchange - if present at all - is insignificant, and that rheogenic HCO₃^- flow with coupling to Na⁺ flow is also absent or insignificant. A transient disturbance of the Na⁺ pump or a transient unspecific increase of the membrane permeability was also excluded by experiments with ouabain and by the observation that SITS (4-acetamido-4'-isothiocyano-2,2' disulphonic stilbene) blocked the HCO₃^- response instantaneously. The data strongly support the notion that the potential changes in response to peritubular HCO₃^- concentration changes arise from passive rheogenic bicarbonate transfer across the peritubular cell membrane, and hence that this membrane has a high conductance for bicarbonate buffer.