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version for printing (Journal of Experimental Zoology,
279:509-520)
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 (delta-H+) in the marine long-horned sculpin (Myoxocephalus octodecimspinosus) following acidosis. Delta-H+ 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 x 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 2x the amount infused. A 30% decrease in plasma Pco2 following the metabolic acidosis in sculpin adapted 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 delta-H+. A reversible inhibition of delta-H+ was also observed in sculpin exposed to either amiloride or HMA during the acidosis. In contrast, low [Cl- ] or DIDS enhanced delta-H+ 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.
This research was supported by NSF RUI-94-19849 to J.B.C.