Ionized magnesium in the homeostasis of cells: intracellular threshold forMg2+ in human platelets

The role of extracellular magnesium ions in the: homoeostasis of intracellu lar ionized magnesium ([Mg2+](i)) in human platelets was studied. For media containing 0.00 to 0.60 mmol/l of extracellular ionized magnesium ([Mg2+]( o)), the mean [Mg2+](i) fluctuated between 533 and 760 mu mol/l. As the [Mg 2+](o) was increased to 1.5 mmol/l, the [Mg2+](i) increased proportionately and peaked at 1470.1 mu mol/l. Additional increase in the [Mg2+](o) from 1 .50 to 6.00 mmol/l resulted in decreased [Mg2+](i) until it equilibrated be tween 739 and 776 mu mol/l. The influx of Mg2+ at [Mg2+](o) of 0.60 and 1.5 0 mmol/l was studied using verapamil, a calcium channel inhibitor, and ouab ain, an inhibitor of the Na/K pump. respectively. The verapamil (15 mmol/l) blocking experiments resulted in a 92.4% inhibition of the Mg2+ influx int o the platelet at a [Mg2+](o) of 1.50 mmol/l. Ouabain (0.5 and 2.5 mmol/l) showed an enhancement effect on the influx of Mg2+ at [Mg2+](o) of 0.60 mmo l/l and no effect at 1.50 mmol/l. The effect of verapamil indicates that io n channels that are homologous to calcium ion channels may he involved in t he influx of Mg2+ into the platelets. The inhibition of Mg2+ influx for [Mg 2+](o) greater than 1.50 mmol/l may illustrate a protective mechanism that attempts to maintain the viability of platelets at abnormally high [Mg2+](o ). These results suggest that there is an intracellular Mg2+ threshold of 1 500 mu mol/l, above which an active mechanism prevents further influx of Mg 2+. (C) 2001 Elsevier Science B.V. All rights reserved.