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Fig. 1. Schematic cellular model of transport processes in the intestinal epithelium of marine teleost fish. Transcellular and/or paracellular fluid absorption is driven by active NaCl transport fueled primarily by the basolateral Na⁺-K⁺-ATPase (), which provides the electrochemical Na⁺ gradient allowing for Na⁺, Cl^- and K⁺ entry across the apical membrane. Two parallel systems, the Na⁺, Cl^- and the Na⁺,K⁺,2Cl^- cotransporters account for Na⁺, K⁺ and a portion of Cl^- absorption, with the remaining Cl^- uptake occurring via anion exchange (AE). The apical AE performs active transport of not only Cl^- but also HCO₃^-, resulting in high luminal HCO₃^- concentrations and highly alkaline intestinal fluids. Endogenous metabolic CO provides cellular HCO^-₂₃ via carbonic anhydrase for the apical anion exchange process, with the resulting H⁺ being extruded across the basolateral membrane via an NHE-like transporter. The H⁺ extrusion across the basolateral membrane is critical for apical HCO₃^- secretion and ultimately relies on the activity of the basolateral Na⁺-K⁺-ATPase. A physical association of AE and carbonic anhydrase II (CAII) might explain how local HCO₃^- concentrations on the luminal side of the apical membrane can reach levels satisfying the thermodynamical conditions necessary for anion exchange. Exchange of a metabolic waste product (CO2), which exerts limited osmotic pressure, in exchange for an electrolyte provides an osmotic drivingforce for cellular water uptake. Basolateral import of HCO₃^- from extracellular fluids appears to also contribute to luminal HCO^-3₃ secretion and may occur via Na⁺:HCO₃^- cotransport (NBC). Based on previous studies summarized in Table 2, fluid absorbed by the intestinal epithelium is hyper-osmotic and highly acidic (values represent means of all studies listed in Table 2). See text for further details.

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