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

Summary

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.