Bicarbonate-dependent chloride absorption in small intestine: Ion fluxes and intracellular chloride activities

Summary

Proximal, stripped segments of small intestine from the urodeleAmphiuma were short-circuited in media containing Na⁺, Cl⁻ and HCO ⁻₃ . Under these conditions there was a large net absorption of Cl⁻, a small net absorption of Na⁺ and a residual flux (J ^R_Net ) consistent with HCO ⁻₃ secretion. Net Cl⁻ absorption correlated with the short-circuit current (I _sc); net Na⁺ absorption correlated negatively withJ ^R_Net . Acetazolamide eliminated theI _sc, lowered Cl⁻ absorption by 50%, and reduced net Na⁺ absorption without alteringJ ^R_Net . Benzolamide inhibited theI _sc without alteringJ ^R_Net . Benzolamide inhibited theI _sc more rapidly when applied on the mucosal surface. Replacement of Na⁺ or HCO ⁻₃ (and CO₂) in the media eliminated theI _sc, net Cl⁻ absorption and the residual flux. Likewise, inclusion of the stilbene SITS in the serosal media eliminated theI _sc, net Cl⁻ absorption and the residual flux. The cytoplasmic activity of Cl⁻ (a ^a _ci ) was determined with single and double-barreled microelectrodes. Thea ^a _ci of villus absorptive cells in normal media was 21.0mm and in excess of that expected on the basis of electrochemical equilibrium of Cl⁻ at the mucosal membrane. Active Cl⁻ accumulation was also observed in the presence of acetazolamide but was eliminated upon replacement of media Na⁺ with choline. The mucosal membrane potential was depolarized upon replacement of media Na⁺. It is concluded that Cl⁻ is actively absorbed into intestinal cells ofAmphiuma by an electrogenic process located in the mucosal membrane. Depending on the level of intracellular HCO ⁻₃ , accumulated Cl⁻ may diffuse passively back into the mucosal media or undergo exchange with bath HCO ⁻₃ at the serosal membrane.