Intestinal HCO 3 − secretion inAmphiuma: Stimulation by mucosal Cl− and serosal Na+

The requirement for Na⁺ and Cl⁻ in the bathing media to obtain a maximal HCO ₃ ⁻ secretory flux ( $J^{HCO_3^ - } $ ) across isolated short-circuitedAmphiuma duodenum was investigated using titration techniques and ion substitution. Upon substitution of media Na⁺ with choline, HCO ₃ ⁻ secretion was markedly reduced. Replacement of media Cl⁻ produced a smaller reduction of $J^{HCO_3^ - } $ . The presence of Cl⁻ enhanced HCO ₃ ⁻ secretion only if Na⁺ was also in the media. Elevation of media Na⁺ or Cl⁻ in the presence of the other ion produced a saturable increase of $J^{HCO_3^ - } $ . In the presence of Na⁺, Cl⁻ stimulated $J^{HCO_3^ - } $ when added to the mucosal but not the serosal medium. In the presence of Cl⁻, Na⁺ elevated $J^{HCO_3^ - } $ when added to the serosal but not the mucosal medium. The ability of mucosal Cl⁻ to stimulate $J^{HCO_3^ - } $ was not apparently dependent on mucosal Na⁺. Simultaneous addition of 10mm Cl⁻ to the Na⁺-free mucosal medium and 10mm Na⁺ to the Cl⁻-free serosal medium stimulated $J^{HCO_3^ - } $ above levels produced by serosal Na⁺ alone. In conclusion, intestinal HCO ₃ ⁻ secretion required mucosal Cl⁻ and serosal Na⁺ and did not involve mucosal NaCl cotransport. The results are consistent with a mucosal Cl⁻ absorptive mechanism in series with parallel basolateral Na⁺−H⁺ and Cl⁻−HCO ₃ ⁻ exchange mechanisms.