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-  Mgi2+ modulates Ca2+ flux in pathophysiologic and physiologic states. Increasing concentrations of Mgi2+ during early ischemia or hypoxia have beneficial effects on L-type Ca2+ channels during stress; i.e., Ca2+ influx is inhibited.
-  Depletion of Mgi2+, as occurs after prolonged ischemia and reperfusion, contributes to progressive Ca2+ over-load and subsequent cell damage (discussed subsequently). In addition, loss of Mgi2+ may promote cystolic Ca2+ overload from intracellular sources: Elevated concentrations of Mgi2+ inhibit efflux of Ca2+ from sarcoplasmic reticulum.

Two mechanisms are believed to be involved in inhibition of Ca2+ current by extracellular Mg2+:
-  effects mediated by cationic screening of fixed negative external surface charges
-  competition with permeant ions (Ca2+) for a site within the channel itself.

Mg2+ and Ischemic-Reperfusion Injury studies in the 1970s showed that myocardial ischemia followed by reperfusion results in cytoplasmic Ca2+ overload. There is now general agreement that during and after periods of ischemia, transmembrane Ca2+ influx occurs by several routes, and that cytoprotective agents, including Mg2+, attenuate the increase in intracellular Ca2+ via multiple mechanisms.