Carr S, Thomas T H, Wilkinson R
Department of Medicine, University of Newcastle upon Tyne, UK.
Clin Chim Acta. 1988 Nov;178(1):51-8. doi: 10.1016/0009-8981(88)90268-9.
Sodium-lithium countertransport is believed to depend on a specific protein and since such proteins usually decline with erythrocyte age it would be expected to be reduced in older cells. In fact, sodium-lithium countertransport increased with ageing, whereas the rate constant of the sodium pump decreased. The increase in sodium-lithium countertransport with erythrocyte ageing was due to a phloretin insensitive component that was not present in young erythrocytes. Raised sodium-lithium countertransport in patients with essential hypertension was due mainly to an increased phloretin sensitive component but the phloretin insensitive component was also higher in middle aged erythrocytes. Amiloride had no effect upon sodium-lithium countertransport or unidirectional sodium influx in cells of any age. This suggests that sodium-lithium countertransport is not a mode of action of the sodium-proton exchanger in the erythrocyte.
