Mechanisms of Acid Extrusion by Two Marine Fishes: The Teleost,Opsanus Beta, and the Elasmobranch,Squalus Acanthias

Rates of efflux of H+ and ammonia from a marine teleost and an elasmobranch were measured. Hypercapnia stimulated H+; efflux from both species, stimulated ammonia efflux from the elasmobranch, and inhibited ammonia efflux from the teleost. In both species the H+; and ammonia efflux were predominantly across the branchial epithelium. In Na+-free sea water, the H+ efflux from both species was completely abolished and the ammonia efflux was inhibited by approximately 50%. Injection of an acid load stimulated H+; efflux, which continued for 2-5 h until more than the injected acid load was excreted. It therefore appears that injection of an acid load also produces a metabolic acid load which must be excreted. The H+ efflux from mineral/metabolic acidotic fish is entirely branchial and dependent upon external Na+. The data support the conclusion that marine teleosts and elasmobranchs possess branchial Na+/NH4+ and Na+/H+; ionic exchange mechanisms and that Na+/H+; exchange plays a major role in the response to acidosis in both groups. The possible evolution of these ionic exchange systems is discussed.