The involvement of H+-ATPase and carbonic anhydrase in intestinal HCO3- secretion in seawater-acclimated rainbow trout.

Pyloric caeca and anterior intestine epithelia from seawater-acclimated rainbow trout exhibit different electrophysiological parameters with lower transepithelial potential and higher epithelial conductance in the pyloric caeca than the anterior intestine. Both pyloric caeca and the anterior intestine secrete HCO(3)(-) at high rates in the absence of serosal HCO(3)(-)/CO(2), demonstrating that endogenous CO(2) is the principal source of HCO(3)(-) under resting control conditions. Apical, bafilomycin-sensitive, H(+) extrusion occurs in the anterior intestine and probably acts to control luminal osmotic pressure while enhancing apical anion exchange; both processes with implications for water absorption. Cytosolic carbonic anhydrase (CAc) activity facilitates CO(2) hydration to fuel apical anion exchange while membrane-associated, luminal CA activity probably facilitates the conversion of HCO(3)(-) to CO(2). The significance of membrane-bound, luminal CA may be in part to reduce HCO(3)(-) gradients across the apical membrane to further enhance anion exchange and thus Cl(-) absorption and to facilitate the substantial CaCO(3) precipitation occurring in the lumen of marine teleosts. In this way, membrane-bound, luminal CA thus promotes the absorption of osmolytes and reduction on luminal osmotic pressure, both of which will serve to enhance osmotic gradients to promote intestinal water absorption.