1990Journal of Experimental BiologyRequires access

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

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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.

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Available 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.

Key concepts: Metabolic alkalosis, Alkalosis, Acid–base homeostasis, Bicarbonate, Chemistry, Excretion, Base (topology), Internal medicine

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