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Am J Physiol Heart Circ Physiol 274: H2085-H2093, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 6, H2085-H2093, June 1998

Mitochondrial Ca2+ uptake, efflux, and sarcolemmal damage in Ca2+-overloaded cultured rat cardiomyocytes

Paavo Korge and Glenn A. Langer

Cardiovascular Research Laboratory, Departments of Physiology and Medicine, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1760

The purpose of this study was to determine mitochondrial Ca2+ accumulation and its possible role in initiation of mitochondrial permeability transition (MPT) and sarcolemmal damage in Ca2+-overloaded cardiomyocytes. Cellular Ca2+ overload, generated secondary to ouabain or p-chloromercuribenzoate-stimulated cell Na+ concentration increase, induced Ca2+ accumulation in mitochondria (~3/4 of total net uptake) as identified by kinetic analysis and verified by use of mitochondrial inhibition. Mitochondrial Ca2+ uptake was followed by a rapid Ca2+ efflux (~1 mmol · kg dry wt-1 · min-1) that can be best explained by efflux via Ca2+-dependent nonspecific pores. Cell ATP concentration was stable during mitochondrial Ca2+ uptake and decreased in parallel with Ca2+ efflux. In addition, sarcolemmal damage was not related to the increase in mitochondrial Ca2+ concentration per se, but rather connected with the extent of Ca2+ efflux from the mitochondria. A decrease in the rate of this Ca2+ efflux, indicating also a decrease in a subpopulation of mitochondria with open pores, was followed by decreased sarcolemmal damage. Both dithiothreitol and cyclosporin A decreased rapid Ca2+ efflux and inhibited sarcolemmal damage, implicating MPT as an important component in the mechanism of sarcolemmal damage.

mitochondrial permeability transition; cyclosporin A; sulfhydryl groups


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