Objective To determine effects of Mg 2+ on potassium current, transient inward current (lti) and Na + Ca 2+
exchange current in isolated ventricular myocytes during hypoxia. Methods Single myocytes were isolated from ventricles of adult guinea pig hearts. The patch clamp technique in whole cell configuration was used to study ionic currents, and experiments were performed in an experimental chamber that allows the cell to be exposed to a sufficiently low O 2 pressure. Results The 10 mmol/L intracellular free Mg 2+ (Mg 2+ i) had no effect on action potential abbreviation under normoxic condition, however, the action potential abbreviation during hypoxia was markedly inhibited in presence of 10 mmol/L Mg 2+ i. The amplitude of hypoxia induced time independent outward K + current was also greatly reduced when applied 10 mmol/L Mg 2+ in pipette solution. In early
reoxygenation, Iti occurred in 73% of myocytes, 10 mmol/L extracellular Mg 2+ during hypoxia and reoxygenation lowered incidence of Iti, 10 mmol/L Mg 2+ could partly inhibit the Na + Ca 2+ exchange current in normoxic condition. Conclusion Intracellular Mg 2+ could block hypoxia induced outward current through ATP sensitive potassium channels. Mg 2+ i plays an important role in preventing depletion of cellular K + and regulates beat to beat cardiac activity. Extracellular Mg 2+ most probably decreases the signs of calcium overload in early reoxygenation by inhibiting Na + Ca 2+ exchange.