The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. III. Branchial exchanges

Abstract

Fluxes of both acidic equivalents (J net H+) and electrolytes across the gills were continuously monitored in the freshwater rainbow trout ( Salmo gairdneri) during 24 h normoxia ( P I O 2 = 120−150 torr; control) , 72 h hyperoxia ( P I O 2 = 500−600 torr ), and 24 h return to normoxia. A highly negative J net H+ ( i.e., excretion) was responsible for over 90% of the compensation of respiratory acidosis induced by hyperoxia in the whole animal. Similarly, a highly positive J net H+ ( i.e., uptake)_accounted for virtually all the compensation of metabolic alkalosis induced by normoxic recovery. Hyperoxia was associated with a small net gain of Na + and large net losses of Cl − at the gills, while normoxic recovery was associated with large net losses of Na + and net gains of Cl −, effects reflected in ECF composition. Unidirectional flux analyses with radiotracers ( 22Na, 36Cl) demonstrated that these net flux alterations resulted from rapid and complex changes in both influx and efflux components such that the difference between J net Na+ and J net Cl− was stoichiometrically equivalent to J net H+. The results support the concept that Na + vs acidic equivalent (H +, NH + 4) and Cl − vs basic equivalent (HCO 3 −, OH −) exchanges at the gill are dynamically adjusted in order to correct internal acid-base disturbances.