Intestinal HCO3− secretion in marine teleost fish: evidence for an apical rather than a basolateral Cl−/HCO3− exchanger

Abstract

Intestinal fluid was collected from 11 marine teleost fish from the Baltic sea and the Pacific ocean. The anterior, mid and posterior segments of the intestine contained 33–110 mM of HCO₃ ⁻ equivalents (with exception of the Atlantic cod which contained only 5–15 mM). Considering literature values of transepithelial potentials and concentration gradients, these high levels of HCO₃ ⁻ equivalents are probably the result of active HCO₃ ⁻ transport. Possible HCO₃ ⁻ transport mechanisms were studied in the Pacific sanddab (Citharichthys sordidus) in vitro. Measurements of net secretion of HCO₃ ⁻ equivalents across the intestinal epithelium revealed mucosal DIDS sensitivity (10⁻⁴ M) and Cl⁻-dependence of the HCO₃ ⁻ equivalent net flux, but no serosal DIDS (10⁻⁴ M) sensitivity. Net Na⁺ uptake was abolished in the absence of Cl⁻, but some Cl⁻ uptake persisted in the absence of Na⁺, at a rate similar to that of net HCO₃ ⁻ secretion. Anterior, mid and posterior segments of the intestine performed similarly. These observations support the presence of an apical rather than a basolateral Cl⁻/HCO₃ ⁻ exchanger and thus contrast the currently accepted model for intestinal HCO₃ ⁻ secretion. This apical Cl⁻/HCO₃ ⁻ exchanger alone, however, is not sufficient for maintaining the observed HCO₃ ⁻ equivalents gradient in vivo. We suggest a coupling of cytosolic carbonic anhydrase, a basolateral proton pump and the apical Cl⁻/HCO₃ ⁻ exchanger to explain the intestinal HCO₃ ⁻ transport.