[Protective effect of magnesium on ionic channels in guinea pig ventricular myocytes during hypoxia]

To determine effects of Mg2+ on potassium current, transient inward current (Iti) and Na(+)-Ca2+ exchange current in isolated ventricular myocytes during hypoxia.

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 O2 pressure.

The 10 mmol/L intracellular free Mg2+ (Mg2+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 Mg2+i. The amplitude of hypoxia-induced time independent outward K+ current was also greatly reduced when applied 10 mmol/L Mg2+ in pipette solution. In early reoxygenation, Iti occurred in 73% of myocytes, 10 mmol/L extracellular Mg2+ during hypoxia and reoxygenation lowered incidence of Iti, 10 mmol/L Mg2+ could partly inhibit the Na(+)-Ca2+ exchange current in normoxic condition.

Intracellular Mg2+ could block hypoxia-induced outward current through ATP sensitive potassium channels. Mg2+i plays an important role in preventing depletion of cellular K+ and regulates beat-to-beat cardiac activity. Extracellular Mg2+ most probably decreases the signs of calcium overload in early reoxygenation by inhibiting Na(+)-Ca2+ exchange.