MECHANISMS OF ACID-BASE EXCRETION ACROSS THE GILLS OF A MARINE FISH

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 exchan ges in fresh water and marine species. We measured the acid-base balan ce and net H+ transfers (Delta H+) in the marine long-horned sculpin ( Myoxocephalus octodecimspinosus) following acidosis. Delta H+ was dete rmined in different groups of acid loaded (2-3 meg kg(-1)) animals whi ch 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 co ntaining 1 x 10(-4) M amiloride, 5-(N,N-hexamethylene)-amiloride (HMA) , or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid(DIDS). Both se awater and 20% SW adapted fish were able to completely compensate for the infused load and over 24 hours typically over-excreted more than 2 x the amount infused. A 30% decrease in plasma P-CO2 following the met abolic 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 necess ary to induce a positive Delta H+. A reversible inhibition of Delta H was also observed in sculpin exposed to either amiloride or HMA durin g the acidosis. In contrast, low [Cl-] or DIDS enhanced Delta H+ excre tion. We conclude that net H+ excretion measured following acidosis in these seawater or brackish water adapted animals is the sum of parall el (and counter acting) apical gill Na+/H+ and Cl-/HCO3- exchanges. Th e Na+/H+ transfers are most likely via an antiporter of the NHE family and occur on the background of continued ''band-3'' Cl-/HCO3- exchang e. (C) 1997 Wiley-Liss, Inc.