The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. III. Branchial exchanges.
Fluxes of both acidic equivalents (JH+net) and electrolytes across the gills were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control), 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. A highly negative JH+net (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 JH+net (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 JNa+net and JCl-net was stoichiometrically equivalent to JH+net. 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.
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D004573:Electrolytes / Q000378:metabolism*; D005260:Female; D005880:Gills / Q000378:metabolism*; D007474:Ion Exchange; D008297:Male; D010100:Oxygen / Q000502:physiology*; D012487:Salmonidae / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D014337:Trout / Q000378:metabolism*
D002712:Chlorides; D004573:Electrolytes; D012964:Sodium; D010100:Oxygen; D002118:Calcium