Although it has been a subject of considerable research, many questions regarding the mechanism(s) of ammonia excretion (JAmm) across fish gills remain unresolved. Recent advances improving our understanding of the linkage between CO2 and ammonia excretion, and the likelihood that H+-ATPases are present in freshwater fish gills, should improve our understanding about mechanisms of branchial JAmm. Moreover, basic differences in gill structure and function between freshwater- and seawater-adapted fishes are probably reflected by dissimilar mechanisms of JAmm. In fresh water, JAmm likely proceeds exclusively by NH3 diffusion down favorable blood-to-expired gill water PNH3 gradients. The carbonic anhydrase-catalyzed hydration of excreted CO2 augments JAmm by generating H+ that trap NH3 (as NH4+) as it diffuses into the gill water. To a lesser extent, the active extrusion of H+, via branchial H+-ATPase's, might also facilitate JAmm. The probable absence of electroneutral Na+/H+ exchange on the apical epithelia, makes branchial Na+/NH4+ exchange unlikely in freshwater fishes. In marine fishes, JAmm likely occurs via passive NH3 diffusion but NH4+ diffusion is also important, owing to the much higher cationic permeability of the gills of seawater fishes. The high Na+ concentrations of seawater indicate that apical Na+/NH4+ exchange is also possible in marine fishes. Finally, substitution of NH4+ for K+ on basolateral Na+:K+ATPase's and/or Na+/2Cl−/K+ co-transporters could also contribute to JAmm by marine fishes.
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