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The effects of alterations in the external sodium concentration on human leucocyte sodium and potassium transport in vitro
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AbstractHuman leucocytes incubated in tissue culture fluid of low‐sodium concentration (2 mM; iso‐osmolarity maintained with choline chloride) reached a new equlibrium within 1 hour and lost approximately 25% of intracellular potassium and 70% of intracellular sodium. The rate constant for ouabainsensitive sodium efflux fell by more than 50% and the ouabain‐insensitive rate constant increased nearly threefold in the low‐sodium medium. Total sodium efflux fell in proportion to internal sodium whereas ouabain‐insensitive sodium efflux remained unchanged. A reduction in external sodium from 140 to 2 mM was associated with a 75% fall in sodium influx. In the low‐sodium medium ouabainsensitive potassium influx exceeded ouabain‐sensitive sodium efflux and no ouabain‐sensitive potassium efflux could be demonstrated. Ouabain‐insensitive potassium influx and that portion of potassium efflux which is dependent on external potassium fell in parallel in low‐sodium cells, suggesting reduced activity of a ouabain‐insensitive K:K exchange system.
Title: The effects of alterations in the external sodium concentration on human leucocyte sodium and potassium transport in vitro
Description:
AbstractHuman leucocytes incubated in tissue culture fluid of low‐sodium concentration (2 mM; iso‐osmolarity maintained with choline chloride) reached a new equlibrium within 1 hour and lost approximately 25% of intracellular potassium and 70% of intracellular sodium.
The rate constant for ouabainsensitive sodium efflux fell by more than 50% and the ouabain‐insensitive rate constant increased nearly threefold in the low‐sodium medium.
Total sodium efflux fell in proportion to internal sodium whereas ouabain‐insensitive sodium efflux remained unchanged.
A reduction in external sodium from 140 to 2 mM was associated with a 75% fall in sodium influx.
In the low‐sodium medium ouabainsensitive potassium influx exceeded ouabain‐sensitive sodium efflux and no ouabain‐sensitive potassium efflux could be demonstrated.
Ouabain‐insensitive potassium influx and that portion of potassium efflux which is dependent on external potassium fell in parallel in low‐sodium cells, suggesting reduced activity of a ouabain‐insensitive K:K exchange system.
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