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

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.