Aldosterone and PCO2 enhance K-dependent chloride absorption in rat distal colon

We have previously demonstrated that, in the absence of Na⁺ in vitro, the rate of colonic K⁺ absorption is increased by increasing PCO₂. Chronic secondary hyperaldosteronism induced by dietary Na-depletion further stimulated K⁺ absorption under these conditions. Because the observed increments in CO₂-dependent K⁺ absorption were not accompanied by corresponding changes in short-circuit current, macroscopic electroneutrality must have been maintained either by anion absorption or by cation secretion. Colonic Cl^– absorption is known to respond to increased PCO₂ both in vivo and in vitro, but its response under Na-free conditions and the relationship to K⁺ absorption have not been examined. To determine the relationship of Cl^– absorption to K⁺, we measured unidirectional fluxes of ³⁶Cl and the response to PCO₂ in voltage-clamped segments of rat distal colon. Our findings indicate that the rate of Cl^– absorption is increased by increasing CO₂, both in the presence and absence of Na⁺. Under Na-free conditions, Cl^– absorption is inhibited by acetazolamide and by the absence of K⁺; K⁺ absorption (⁸⁶Rb or ⁴²K flux) is inhibited in a reciprocal fashion by the absence of Cl^–. The rates of K⁺ and Cl^– absorption are similar in controls and after secondary hyperaldosteronism due to a Na-deficient diet. These findings suggest that K⁺ and Cl^– absorption are closely coupled under Na-free conditions, most likely due to the operation of parallel, aldosterone-responsive H⁺-K⁺ and Cl^–-HCO₃^–exchange pathways.