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Variable coupling of active NA + + K + transport in Ehrlich ascites tumor cells: Regulation by external NA + and K +
Author(s) -
Smith Thomas C.,
Robinson Susan C.
Publication year - 1981
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041060310
Subject(s) - sodium , potassium , chemistry , analytical chemistry (journal) , isotopes of sodium , nuclear chemistry , chromatography , organic chemistry
Abstract The effects of altered external sodium and potassium concentrations on steady state, active Na + + K + transport in Ehrlich ascites tumor cells have been investigated. Membrane permeability to Na + and K + , intracellular [Na + ] and [K + ], and membrane potential were measured. Active cation fluxes were calculated as equal and membrane potential were measured. Active cation fluxes were calculated as equal and opposite to the net, diffusional leak fluxes. Elevation of external K + (6–60 Mm)by equivalent replacement of Na + (154–91 mM) inhibits both active Na + and K + fluxes, but not proportionally. This results in a decrease of the coupling ratio (r p = ‐J k p /J p Na ) as external K + is increased. Elevation of external K + (3–68 mM) at constant Na + (92mM) inbibits J p k , but is without effect on J p Na . The coupling ratio declines from 1.01 ± 0.14 to 0.07 ± 0.05, a 14‐fold alteration. Reduction of external Na + (154–25 mM) at constant K + (6mM) depresses J p Na , but is without effect on J p k . The coupling ratio increases from 0.63 ± 0.04 at 154 mM Na + to 4.5 ± 2.04 at 25 mM Na + . The results of this investigation are consistent with the independent regulation of active cation fluxes by the transported species. Kinetic analysis of the data indicates that elevation of external sodium stimulates active sodium efflux by interacting at “modifier sites” at the outer cell surface. Similarly, external potassium inhibits active potassium influx by interaction at separate modifier sites.