Anion exchange contributes significantly to intestinal Cl(-) absorption in marine teleost fish and is thus vital for successful osmoregulation. This anion exchange process leads to high luminal HCO(3)(-) concentrations (up to approximately 100 mmol l(-1)) and high pH and results in the formation of CaCO(3) precipitates in the intestinal lumen. Recent advances in our understanding of the transport processes involved in intestinal anion exchange in marine teleost fish include the demonstration of a role for the H(+)-pump (V-ATPase) in apical H(+) extrusion and the presence of an electrogenic (nHCO(3)(-)/Cl(-)) exchange protein (SLC26a6). The H(+)-V-ATPase defends against cellular acidification, which might otherwise occur as a consequence of the high rates of base secretion. In addition, apical H(+) extrusion probably maintains lower HCO(3)(-) concentrations in the unstirred layer at the apical surface than in the bulk luminal fluids and thus facilitates continued anion exchange. Furthermore, H(+)-V-ATPase activity hyperpolarizes the apical membrane potential that provides the driving force for apical electrogenic nHCO(3)(-)/Cl(-) exchange, which appears to occur against both Cl(-) and HCO(3)(-) electrochemical gradients. We propose that a similar coupling between apical H(+) extrusion and nHCO(3)(-)/Cl(-) exchange accounts for Cl(-) uptake in freshwater fish and amphibians against very steep Cl(-) gradients.