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  • 1
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 106 (1981), S. 407-418 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: 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 (rp = -Jkp/JpNa) as external K+ is increased. Elevation of external K+ (3-68 mM) at constant Na+ (92mM) inbibits Jpk, but is without effect on JpNa. 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 JpNa, but is without effect on Jpk. 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.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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