Acid–base regulation in fishes: cellular and molecular mechanisms

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Abstract
The mechanisms underlying acid–base transfers across the branchial epithelium of fishes have been studied for more than 70 years. These animals are able to compensate for changes to internal pH following a wide range of acid–base challenges, and the gill epithelium is the primary site of acid–base transfers to the water. This paper reviews recent molecular, immunohistochemical, and functional studies that have begun to define the protein transporters involved in the acid–base relevant ion transfers. Both Na+/H+ exchange (NHE) and vacuolar‐type H+‐ATPase transport H+ from the fish to the environment. While NHEs have been thought to carry out this function mainly in seawater‐adapted animals, these proteins have now been localized to mitochondrial‐rich cells in the gill epithelium of both fresh and saltwater‐adapted fishes. NHEs have been found in the gill epithelium of elasmobranchs, teleosts, and an agnathan. In several species, apical isoforms (NHE2 and NHE3) appear to be up‐regulated following acidosis. In freshwater teleosts, H+‐ATPase drives H+ excretion and is indirectly coupled to Na+ uptake (via Na+ channels). It has been localized to respiratory pavement cells and chloride cells of the gill epithelium. In the marine elasmobranch, both branchial NHE and H+‐ATPase have been identified, suggesting that a combination of these mechanisms may be utilized by marine elasmobranchs for acid–base regulation. An apically located Cl−/HCO3− anion exchanger in chloride cells may be responsible for base excretion in fresh and seawater‐adapted fishes. While only a few species have been examined to date, new molecular approaches applied to a wider range of fishes will continue to improve our understanding of the roles of the various gill membrane transport processes in acid–base balance.