GROSELL, M.; WILSON, R.; RSMAS, Univ. of Miami, Fl; Univ. of Exeter, UK: Intestinal chloride/bicarbonate exchange is involved in osmoregulation

Marine teleosts combat dehydration by drinking. In addition to apical Na⁺:Cl^– and Na⁺:K⁺:2Cl^– co-transport, Cl^–/HCO₃^– exchange is involved in intestinal Cl^– and water absorption. This exchange enables water and Cl^– absorption in absence of luminal Na⁺ and can account for up to 50% of intestinal Cl^– absorption. A consequence of this anion exchange is high [HCO₃^–] (> 100 mM) and high pH (>8.5) in the intestinal fluids. Considering the electrochemical gradients for both Cl^– and HCO₃^– across the intestinal epithelium of most species, the Cl^–/HCO₃^– exchange perform active transport of both anions. The source of HCO₃^– is carbonic anhydrase mediated hydration of CO₂ and apical anion exchange seems to be fueled by active extrusion of H⁺ across the basolateral membrane. In some species, intestinal HCO₃^– secretion exhibits serosal Na⁺ dependence and amiloride sensitivity suggesting H⁺ extrusion via a Na⁺/H⁺ exchange mechanism. In these species, active HCO₃^– secretion (and Cl^– absorption) is fueled by the electrochemical Na⁺ gradient created by the Na/K-ATPase. In the European flounder (Platichthys flesus), however, HCO₃^– secretion is insensitive to serosal amiloride and not dependent on serosal sodium, suggesting active proton extrusion via a basolateral H⁺ ATPase. As a result of the alkalinity in the intestinal lumen and the high Ca²⁺ concentration in seawater, substantial precipitation of CaCO₃ occurs in the intestine. This is advantageous to marine teleosts because 1) it reduces intestinal Ca²⁺ uptake and thus the need for renal Ca²⁺ excretion and 2) it lowers the osmolality of the intestinal fluids aiding in fluid absorption. Intestinal bicarbonate secretion is stimulated by elevated luminal Ca²⁺ in the mM range suggesting the involvement of an apical membrane-bound Ca²⁺ sensing receptor (CaR).