Chloride distribution in the proximal convoluted tubule ofNecturus kidney

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Abstract
To assess the mechanism(s) by which intraluminal chloride concentration is raised above equilibrium values, intracellular Cl− activity (α i Cl ) was studied in the proximal tubule ofNecturus kidney. Paired measurements of cell membrane PD (V BL) and Cl-selective electrode PD (V BL Cl ) were performed in single tubules, during reversible shifts of peritubular or luminal fluid composition. Steadystate α i Cl was estimated at 14.6±0.6 mmol/liter, a figure substantially higher than that predicted for passive distribution. To determine the site of the uphill Cl− transport into the cell, an inhibitor of anion transport (SITS) was added to the perfusion fluid. Introduction of SITS in peritubular perfusate decreased α i Cl , whereas addition of the drug in luminal fluid slightly increased α i Cl ; both results are consistent with basolateral membrane uphill Cl− transport from interstitium to the cell. TMA+ for Na+ substitutions in either luminal or peritubular perfusate had no effect on α i Cl . Removal of bicarbonate from peritubular fluid, at constant pH (a situation increasing HCO 3 − outflux), resulted in an increase of α i Cl , presumably related to enhanced Cl− cell influx: we infer that Cl− is exchanged against HCO 3 − at the basolateral membrane. The following mechanism is suggested to account for the rise in luminal Cl− concentration above equilibrium values: intracellular CO2 hydration gives rise to cell HCO 3 − concentrations above equilibrium. The passive exit of HCO 3 − at the basolateral membrane energizes an uphill entry of Cl− into the cell. The resulting increase of α i Cl , above equilibrium, generates downhill Cl− diffusion from cell to lumen. As a result, luminal Cl− concentration also increases.