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.