Na+ and Cl− Uptake Kinetics, Diffusive Effluxes and Acidic Equivalent Fluxes Across the Gills of Rainbow Trout II. Responses to Bicarbonate Infusion
Greg G. Goss, Chris M. Wood
Abstract
Greg G. Goss, Chris M. Wood
Abstract
ABSTRACT Adult rainbow trout fitted with arterial and bladder catheters were chronically infused with either bicarbonate (as NaHCO3) or NaCl for 19 h at approximately 410μequivkg−1h−1. NaHCO3 infusion produced a pure exogenous metabolic alkalosis of approximately 0.35 pH units accompanied by a decrease in plasma [Cl−] but no change in plasma [Na+]. Alkalosis stimulated Cl− influx and inhibited Na+ influx (measured at 10-16h infusion), resulting in a negative Na+ balance, a positive Cl− balance and a large net basic equivalent excretion (=acidic equivalent uptake) across the gills. The latter was approximately equal to the rate of HCO3−loading. The kidney accounted for approximately 13 % of the acid-base compensation. Kinetic analysis revealed that reductions in were accomplished by increases in (463μuquivl−1; NaHCO3-infused vs 276μequivl−1; NaCl-infused) and large decreases in (262μequivkg−1h−1 vs 689μequivkg−1 h−1) while stimulation of was accomplished by large increases in only (674 μequiv kg−1 h−1 vs 360μequivkg−1 h−1). Thus, Jmax can be increased or decreased in response to acid-base disturbance, but Km can only be increased; the Na+ and Cl− carriers operate close to maximum affinity under control conditions. Basic equivalent excretion was described by a virtually identical kinetic curve to that of the Cl− uptake. NaHCO3 infusion also induced a differential diffusive efflux of Na+ over Cl− which could account for up to 35 % of the acid-base compensation during alkalosis.
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ABSTRACT Adult rainbow trout fitted with arterial and bladder catheters were chronically infused with either bicarbonate (as NaHCO3) or NaCl for 19 h at approximately 410μequivkg−1h−1. NaHCO3 infusion produced a pure exogenous metabolic alkalosis of approximately 0.35 pH units accompanied by a decrease in plasma [Cl−] but no change in plasma [Na+]. Alkalosis stimulated Cl− influx and inhibited Na+ influx (measured at 10-16h infusion), resulting in a negative Na+ balance, a positive Cl− balance and a large net basic equivalent excretion (=acidic equivalent uptake) across the gills. The latter was approximately equal to the rate of HCO3−loading. The kidney accounted for approximately 13 % of the acid-base compensation. Kinetic analysis revealed that reductions in were accomplished by increases in (463μuquivl−1; NaHCO3-infused vs 276μequivl−1; NaCl-infused) and large decreases in (262μequivkg−1h−1 vs 689μequivkg−1 h−1) while stimulation of was accomplished by large increases in only (674 μequiv kg−1 h−1 vs 360μequivkg−1 h−1). Thus, Jmax can be increased or decreased in response to acid-base disturbance, but Km can only be increased; the Na+ and Cl− carriers operate close to maximum affinity under control conditions. Basic equivalent excretion was described by a virtually identical kinetic curve to that of the Cl− uptake. NaHCO3 infusion also induced a differential diffusive efflux of Na+ over Cl− which could account for up to 35 % of the acid-base compensation during alkalosis.
Key concepts: Metabolic alkalosis, Alkalosis, Acid–base homeostasis, Bicarbonate, Chemistry, Excretion, Base (topology), Internal medicine