Mechanisms of acid-base excretion across the gills of a marine fish

Abstract

Na+/H+ and Cl–/HCO3–exchanges in the branchial epithelium are thought to be primarily responsible for acid-base transfers in fish. Several different cellular mechanisms have been proposed to drive these exchanges in fresh water and marine species. We measured the acid-base balance and net H+ transfers (ΔH+) in the marine long-horned sculpin (Myoxocephalus octodecimspinosus) following acidosis. ΔH+ was determined in different groups of acid loaded (2–3 meq kg–1) animals which were: 1) adapted to seawater (SW); 2) adapted to 20% SW; 3) exposed to water with artificially low [Na+] or [Cl–]; 4) exposed to water containing 1 × 10–4 M amiloride, 5-(N,N-hexamethylene)-amiloride (HMA), or 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS). Both seawater and 20% SW adapted fish were able to completely compensate for the infused load and over 24 hours typically over-excreted more than 2× the amount infused. A 30% decrease in plasma PCO2 following the metabolic acidosis in sculpin adpated to 20% SW (presumably secondary to respiratory alterations) contributed to the rapid recovery of blood pH. Low ambient [Na+] reversed normal acid excretion to an uptake (HCO3– loss; even after acid infusion). 20–30 mM Na+ in the water was necessary to induce a positive ΔH+. A reversible inhibition of ΔH+ was also observed in sculpin exposed to either amiloride or HMA during the acidosis. In contrast, low [Cl–] or DIDS enhanced ΔH+ excretion. We conclude that net H+ excretion measured following acidosis in these seawater or brackish water adapted animals is the sum of parallel (and counter acting) apical gill Na+/H+ and Cl–/HCO3– exchanges. The Na+/H+ transfers are most likely via an antiporter of the NHE family and occur on the background of continued “band-3” Cl–/HCO3– exchange. J. Exp. Zool. 279:509–520, 1997.© 1997 Wiley-Liss, Inc.