AJP - Cell Physiology, Vol 267, Issue 2 C633-C641, Copyright © 1994 by American Physiological Society

ARTICLES

Elevated extracellular Mg2+ increases Mg2+ buffering through a Ca-dependent mechanism in cardiomyocytes

K. L. Koss and R. D. Grubbs
Department of Pharmacology and Toxicology, School of Medicine, Wright State University, Dayton 45435.

To investigate the physiological basis for the pharmacological action of extracellular magnesium (Mg2+O), cultured ventricular myocytes were exposed to either 0.8 mM (physiological) or 5.0 mM Mg2+ (therapeutic concentration) in the presence and absence of metabolic inhibitors. Metabolic inhibition, induced with 1 mM iodoacetate and 1 mM NaCN, was used to liberate Mg2+ from MgATP into the myoplasm, permitting examination of the role of elevated Mg2+O on myoplasmic Mg2+ buffering. The increase in Mg2+ activity observed in the presence of 5 mM Mg2+O was diminished compared with that observed in cells exposed to 0.8 mM Mg2+O. Furthermore, the increase in myoplasmic Mg2+ activity observed in the presence of 5 mM Mg2+O was identical to that reported previously in the absence of extracellular Ca2+. Fura 2 measurements of Ca2+ activity in these experimental conditions suggested that the Ca2+ permeability of cells conditions suggested that the Ca2+ permeability of cells exposed to 5 mM Mg2+ was less than that observed for cells exposed to 0.8 mM Mg2+. Using the Mg2+ buffer coefficient to quantitate cellular Mg2+ buffering, we observed a 63% increase in Mg2+ buffering in cells exposed to 5 mM Mg2+ compared with cells exposed to 0.8 mM Mg2+. This study demonstrates that elevated Mg2+O alters cardiomyocyte myoplasmic Mg2+ activity as the result of increased Mg2+ buffering through a Ca(2+)-sensitive mechanism.

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