ABSTRACT
Endogenous respiratory acidosis and metabolic alkalosis were induced in bladder-catheterized freshwater rainbow trout by exposure to environmental hyperoxia (72 h) and its subsequent removal. Unidirectional and net fluxes of Na+, Cl− and acidic equivalents across the gills were examined over 0.5 h intervals. Hyperoxia resulted in a positive Na+ balance, negative Cl− balance and net acidic equivalent excretion. Return to normoxia caused a negative Na+ balance, a positive Cl− balance and net basic equivalent excretion (=acidic equivalent uptake). Cl−/basic equivalent exchange was more important than Na+/acidic equivalent exchange in the homeostatic responses, and alkalosis was a more potent stimulus than acidosis for change in branchial ion fluxes. Kinetic analysis demonstrated that alterations in ion fluxes were achieved by complex changes in both the Km (inverse of affinity) and the Jmax (maximal transport rate) of the branchial C1−/HCO3− (OH−) and Na+/H+(NH4+) transporters. (control=165μequivl−1) and
114μequivl−1) were increased during hyperoxic acidosis to 250 and 44μ μequivl−1, respectively.
(291μequiv kg−1h−1) and
(456 μequiv kg−1 h−1) did not change significantly. During post-hyperoxic alkalosis,
was further increased to 559μequivl−1,
increased to 445μequivkg−1h−1, while
and
decreased to 137μequivl−1 and 309μequiv kg−1 h−1, respectively. Diffusive efflux was examined using a novel method. There was no significant differential diffusive efflux of Na+ and Cl− during hyperoxia but diffusive Na+ efflux exceeded Cl− efflux during posthyperoxic alkalosis, thereby serving as an additional mechanism for basic equivalent excretion.