Abstract
The rate of luminal alkalinization in vitro by Gillichthys mirabilis posterior intestine as measured by a manual pH stat technique was 0.70 +/- 0.05 mu Equiv/cm2 h; acidification of the mucosal medium was never observed. The rate of HCO-3 secretion (JHCO3) was reduced by ouabain, serosally-applied DIDS, removal of serosal HCO3- and replacement of media Cl- with gluconate. HCO3- secretion was enhanced by replacement of Cl- with isethionate and unaffected by mucosal DIDS, furosemide or acetazolamide. JHCO3 was reduced at mucosal pH above or below 7.5. These results support active HCO3- secretion via a Cl-/HCO3- exchange mechanism on the basolateral membrane and a conductive exit pathway for HCO-3, H+ or OH- on the apical membrane.
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