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Mechanisms of Acid Extrusion by Two Marine Fishes: The Teleost, Opsanus Beta, and the Elasmobranch, Squalus Acanthias
1 Department of Biology, University of Miami, Coral Gables, FL 33124, U.S.A. Mt. Desert Island Biological Laboratory, Salsbury Cove, ME 04672, U.S.A.; Department of Zoology, University of Florida, Gainesville, FL 32611, U.S.A.
1. Rates of efflux of H+ and ammonia from a marine teleost and an elasmobranch were measured.
2. Hypercapnia stimulated H+ efflux from both species, stimulated ammonia efflux from the elasmobranch, and inhibited ammonia efflux from the teleost.
3. 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%.
4. 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.
5. The H+ efflux from mineral/metabolic acidotic fish is entirely branchial and dependent upon external Na-.
6. 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.
7. The possible evolution of these ionic exchange systems is discussed.
Submitted on June 1, 1981
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