Electrophysiological analysis of bicarbonate permeation across the peritubular cell membrane of rat kidney proximal tubule. II. Exclusion of HCO3(-)-effects on other ion permeabilities and of coupled electroneutral HCO3(-)-transport.

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 SO4(2-) 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.