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

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Abstract
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.