Claiborne, J. B. (1998). Acid-Base Regulation. In "The Physiology of Fishes" (D. H. Evans, Ed.), CRC Press, Boca Raton, 179-200.

This is a figure from the chapter. The book is now available.

Figure 9.

Model for mechanisms of acid-base exchanges in seawater fishes following acidosis.

H⁺ excretion is increased by an insertion of additional Na⁺/H⁺ antiporter (NHE) in the apical membrane. Dehydration of ammonium transferred by basolateral Na⁺-K⁺-ATPase (or ionic diffusion) also contributes to net H+ excretion. HCO₃^- loss via band-3 Cl^-/HCO₃- exchange continues even during acidosis. H⁺ and HCO₃- are generated within the cell from the hydration of CO₂ catalyzed by carbonic anhydrase. Under control conditions, the rates of H⁺ and HCO₃- excretion are nearly equal. The specific cellular type(s) responsible for the acid-base exchanges in the seawater gill is unknown at present - while the model shows all exchanges taking place in the CC, the contribution of the PVCs to acid-base exchanges is also likely. Filled circles represent ATPases, empty circles are exchanges that do not require ATP directly. Dashed lines represent diffusive movement. For clarity, CC osmoregulatory exchanges have been omitted from the model. CA=carbonic anhydrase; CC=chloride cell, ECF=extracellular fluid.