Effect of external magnesium on intracellular free sodium:: Na+ flux via Na+/Mg2+ antiport is masked by other Na+ transport systems in rat cardiac myocytes

Mg2+ efflux from heart cells on a Na+/Mg2+ antiport has been postulated, but the Na+ flux component of the antiport has not been demonstrated. The study aimed to establish if the Na+ flux component could be measured by following changes in [Na+](i) with SBFI during conditions known to reverse the antiport (5 mmoI/L Mg-0(2+), Na-0(+)- & Ca-0(2+)-free); and after minimising the activity of other Na+ transport pathways. Resting [Na+](i) was 8 +/- 0.7 mmol/L (mean +/- S.E., n = 39 cells] in normal Tyrode's solution. [Na+](i) decreased below the normal level in all cells (a decline of 4-5 mmol/L, n = 21) during perfusion with 5 mmol/L Mg-0(2+) (Na-0(+)- & Ca-0(2+)-free). Controls using I mmol/L Mg-0(2+) showed similar declines in [Na+](i), but the fall was greatest when Na-0(+) was replaced by K-0(+) (decline of 6 mmol/L] rather than the tetramethylammonium ion (TMA(+)). The rate of decrease in [Na+](i) during perfusion with 5 mmol/L Mg-0(2+) (Na-0(+)- & Ca-0(2+)-free] was slowed by 20 muM ouabain (n = 5) or by elevation of pH, to pH 9 (n = 7) so that [Na+](i) remained close to the initial value. The decrease of [Na+](i) was not affected by 10 muM imipramine (n = 15). These data suggest that the Na+ efflux component of the Na+/Mg2+ antiport is masked in Na-0(+)- and Ca-0(2+)-free conditions by other Na-i(+) efflux pathways.