“…Sodium entry must also be through calcium channels, which are known to lose their specificity under low calcium conditions (Tunstall et al, 1986) since cadmium and nickel, two well-described calcium channel blockers (Frank et al, 1982;Rich and Langer, 1982), prevent the paradoxical increase as well. The depolarization caused by low external calcium (Almers et al, 1984;Minota and Koketsu, 1983) and intracellular sodium loading by either means are, however, apparently able to shift the exchanger into its reverse phase when it is reactivated by external calcium during reperfusion (Caputo et al, 1989;DiPolo and Beauge, 1988).…”