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Effects of Magnesium on Cardiac Excitation-Contraction Coupling

Anushka P. Michailova, PhD, Mary Ellen Belik and Andrew D. McCulloch, PhD

Department of Bioengineering, University of California San Diego, La Jolla CA, USA



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Fig. 1. Model outputs in response to 1-Hz pulse train (9–10 s). Panels A–B, D–F: Free Mg2+ 1 mM (solid line), 0.5 mM (dash-dot line), 0.3 mM (dotted line), 0.2 mM (dash line), 0.1 mM (dash-dot-dot line). Bottom trace in (D) shows an expanded view of the peak of L-type Ca2+ current at different [Mg2+]i. Panel C: Free Mg2+ 1 mM (solid line), 3 mM (dotted line), 5 mM (dash line). [ATP]tot 7 mM, [ADP]tot 5 µM.

 


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Fig. 2. Adding ATP and ADP as mobile Ca2+ and Mg2+ buffers slightly shorten the action potential (9–10 s). ATP, ADP and Mg2+ not included (dash-dot line). Normal conditions: [ATP]tot 7 mM, [ADP]tot 5 µM, [Mg2+]i 1 mM (solid line). Metabolic inhibition: [ATP]tot 3 mM, [ADP]tot 3 mM, [Mg2+]i 2.25 mM (dash-dot-dot line).

 





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