Carbonic anhydrase facilitates CO2 and NH3 transport across the sarcolemma of trout white muscle.

An isolated, perfused tail preparation was used to study the role of carbonic anhydrase (CA) in CO2 and NH3 transport across the sarcolemma of white muscle in the rainbow trout. Tissue was perfused with either control saline or saline containing the CA inhibitors quaternary ammonium sulfanilamide (QAS) or acetazolamide (Az). Inhibition of extracellular CA by QAS reduced CO2 efflux by approximately 30% and caused a significant increase in intracellular PCO2. Inhibition of total muscle CA activity (extracellular and intracellular) by Az also caused a reduction in CO2 efflux, but selective inhibition of intracellular CA only had no effect. Inhibition of both extracellular and intracellular CA activity resulted in increases in total intracellular ammonia concentrations, intracellular NH3 partial pressure (PNH3) and an increased PNH3 gradient across the sarcolemma. This suggests that both extracellular and intracellular CA function in normal NH3 transport out of the muscle. We suggest that CA in the extracellular boundary layer facilitates CO2 transport via the catalyzed hydration of CO2, thus maintaining the PCO2 gradient across the sarcolemma. H ions produced by that reaction serve to protonate excreted NH3, which helps maintain the PNH3 gradient. Thus CO2 and NH3 excretion are linked by the action of CA.