Acidic Ca(2+) stores in platelets.

Changes in cytosolic free Ca(2+) concentration play a pivotal role in the regulation of platelet functions, from secretion of autocrine and procoagulant factors to reversible or irreversible aggregation. It has long been recognized that platelet agonists release Ca(2+) accumulated into the dense tubular system, the analogue of the endoplasmic reticulum. However, current evidence indicates that Ca(2+) can also be stored and released from a number of acidic organelles, including lysosomes and lysosome-related organelles. Ca(2+) release from the dense tubular system is mediated through phospholipase C-dependent synthesis of inositol 1,4,5-trisphosphate, whereas Ca(2+) efflux from the acidic stores seems to be associated to the second messenger nicotinic acid adenine dinucleotide phosphate. The biochemical and biophysical properties of both Ca(2+) stores in platelets have been reported to show significant differences. Selective discharge of one or both stores depends on the platelet agonist and the concentration used, which further supports the complexity of the Ca(2+) signals that regulate platelet function. In this paper, we summarize the current knowledge on the role of acidic organelles in agonist-evoked Ca(2+) mobilization and highlight recent progress in understanding the functional aspects of the acidic Ca(2+) stores in Ca(2+) signalling and platelet physiology.