Differential Approaches to Blood Acid-Base Regulation during Exposure to Prolonged Hypercapnia in Two Freshwater Teleosts: The Rainbow Trout (Salmo gairdneri) and the American Eel (Anguilla rostrata)

The effects of external hypercapnia (0.8% CO₂ in air) on blood acid-base variables were examined in the eel (Anguilla rostrata) and in the trout (Salmo gairdneri). Both species were able topartially regulate whole-bloodpH during hypercapnia owing to similar elevations ofplasma [HCO₃-]. In the trout, the ability to regulate whole-blood pH was attributed primarily to a reduction in the activity of branchial Cl⁻/HCO₃-exchange, whereas, in the eel, pH regulation was due entirely to stimulation of branchial Na⁺/H⁺ exchange. Acclimation of eels to increased external [NaCl] (2 mM) caused a significant blood alkalosis; branchial Na⁺ uptake was markedly stimulated (from 34 to 921 μmol kg⁻¹ h⁻¹), while Cl⁻ uptake remained at exceptionally low levels (5-6μmol kg⁻¹ h⁻¹). However, the ability to regulate hypercapnic acidosis in eels acclimated to high [NaCl] water was unchanged. Eels also were acclimated to low external [Na⁺] (Na⁺ = 0.0090 ± 0.0003 mM; Cl⁻ = 0.162 ± 0.017 mM), which resulted in a significant decrease in whole-blood pH. Branchial Na⁺ uptake was markedly reduced (from 34 to 8 μ mol kg⁻¹ h⁻¹), and the ability to compensate hypercapnic acidosis was abolished. These data indicate that, unlike the trout, the eel relies solely on adjustments of branchial Na⁺ uptake for blood acid-base regulation during hypercapnic acidosis owing to uniquely low and inflexible rates of gill unidirectional Cl⁻ fluxes.