Objective: Magnesium regulates a large number of cellular processes. Small changes in intracellular free Mg(2+) ([Mg(2+)](i)) may have important effects on cardiac excitability and contractility. We investigated the effects of [Mg(2+)](i) on cardiac excitation-contraction coupling.
Methods: We used our ionic-metabolic model that incorporates equations for Ca(2+) and Mg(2+) buffering and transport by ATP and ADP and equations for MgATP regulation of ion transporters (Na(+)-K(+) pump, sarcolemmal and sarcoplasmic Ca(2+) pumps).
Results: Model results indicate that variations in cytosolic Mg(2+) level might sensitively affect diastolic and systolic Ca(2+), sarcoplasmic Ca(2+) content, Ca(2+) influx through L-type channels, efficiency of the Na(+)/Ca(2+) exchanger and action potential shape. The analysis suggests that the most important reason for the observed effects is a modified normal function of sarcoplasmic Ca(2+)-ATPase pump by altered diastolic MgATP levels.
Conclusion: The model is able to reproduce qualitatively a sequence of events that correspond well with experimental observations during cardiac excitation-contraction coupling in mammalian ventricular myocytes.