Effects of Calcium Antagonists on Injured Cells
In recent years, calcium has been recognized as a key messenger in the regulation of a variety of cellular processes (1). The regulatory role of calcium depends upon a low cytosolic calcium ionic activity which is maintained by energy-requiring transport mechanisms operating at the level of the membranous organelles. During cell activation, the cytosolic calcium activity rises transiently and calcium alters metabolic reactions by binding to specific receptors such as troponin-C, calmodulin, parvalbumin and others (1). In many cells, activation has been shown to be associated with a transmembrane inward flux of calcium, although release of internally stored calcium may importantly contribute to the rise in cytosolic calcium (2). For a cell to maintain its normal electrolyte composition and excitability, a coordinated extrusion of calcium must follow net uptake. Whereas electrophysiological studies have provided considerable information about the influx of calcium through specific membrane pores, the transport mechanisms responsible for the extrusion of calcium are less well understood (2). It has been assumed that accumulation of calcium in injured cells reflects predominantly a passive inward leak of calcium through damaged cell membranes. However, another hypothesis is that the initial accumulation of calcium in injured cells is not caused by some gross inward electrolyte leak, but reflects instead an impaired uphill transport of calcium.
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