Electrophysiological analysis of bicarbonate permeation across the peritubular cell membrane of rat kidney proximal tubule

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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 SO 4 2− , isethionate, or gluconate. Under those conditions the cell membrane response to HCO 3 − was essentially preserved. In addition it was observed that peritubular Cl− conductance is negligibly small, that Cl−/HCO 3 − exchange — if present at all — is insignificant, and that rheogenic HCO 3 − 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 HCO 3 − response instantaneously. The data strongly support the notion that the potential changes in response to peritubular HCO 3 − 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.