In order to maintain low intracellular Mg(2+) concentration ( [Mg(2+)] (i)), Mg(2+) has to be extruded from cell interior by active transport. In this article, properties of the active Mg(2+) transport in cardiac myocytes are reviewed. After [Mg(2+)] (i) was increased in the solution containing high Mg(2+) concentration, the reduction of extracellular Mg(2+) concentration ( [Mg(2+)] (o)) down to 1 mM caused a rapid decrease in [Mg(2+)] (i) only in the presence of extracellular Na(+);extracellular Na(+) stimulates the Mg(2+) efflux in a concentration dependent fashion with half maximal activation at 53 mM. When the rate of Mg(2+) efflux was compared under different levels of intracellular Na(+) concentration ( [Na(+)] (i)), intracellular Na(+) loading by ouabain decreased the rate of Mg(2+) efflux with 50% inhibition at - 40 mM [Na(+)] (i). In the experiments where the myocytes were voltage clamped at - 80 mV using the perforated patch-clamp technique with amphotericin B, the increase in pipette Na(+) concentration from 0 mM to 130 mM significantly decreased the rate of Mg(2+) efflux. The rate of Mg(2+) efflux was greater at the higher initial levels of [Mg(2 + )] (o), and was nearly zero at the basal levels;the efflux was half activated at 1.9 mM [Mg(2+)] (i). The Mg(2+) efflux was significantly slower at higher [Mg(2+)] (o) (50% inhibition at 10 mM). These results are consistent with the Mg(2+) efflux activity driven by the [Na(+)] gradient across cell membrane, or the Na(+)-Mg(2+) exchange.