Extracellular HCO3- stimulates colonic net Cl- absorption in part by inhibiting basal Cl- secretion. This inhibition was investigated by measuring serosal-to-mucosal Cl- flux across short-circuited colonic segments from Sprague-Dawley rats. Mucosal intracellular pH and bicarbonate were estimated using the pH-sensitive dye BCECF. When extracellular [HCO3post-] ([HCO3post-]e) was increased from 0 to 39 mmol/L at Pco2 33 mm Hg, mucosal intracellular [HCO3post-] ([HCO3post-]i) increased to 25.3 mmol/L and serosal-to-mucosal Cl- flux decreased from 13.0 to 7.1 μEq · cm-2 · h-1. When Pco2 was increased to 72 mm Hg at [HCO3post-]e 39 mmol/L, [HCO3post-]i increased to 29.8 mmol/L and serosal-to-mucosal Cl- flux decreased to 5.9 μEq · cm-2 · h-1. In Ringer's solution containing 21 mmol/L HCO3post- and 20 mmol/L Cl- (but not 100 mmol/L Cl-), increasing Pco2 from 21 to 70 mm Hg increased [HCO3post-]i to 22.6 mmol/L and decreased serosal-to-mucosal Cl- flux from 3.0 to 1.7 μEq · cm-2 · h-1. Overall, serosal-to-mucosal Cl- flux was inversely related to [HCO3post-]i on either side of an [HCO3post-]i plateau of 9-18 mmol/L at which flux was stable. These data suggest that [HCO3post-]i is an important modulator of basal Cl- secretion in rat distal colon.
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