Abstract
Publisher Summary This chapter discusses the nitric oxide and superoxide detection in human platelets. Activation and recruitment of platelets is tightly regulated. Adhesion of platelets to normal endothelium is prevented by several mechanisms, including endothelial cell production of prostacyclin and nitric oxide (NO . ). Nitric oxide inhibits platelet aggregation and prevents thrombosis in a model of endotoxins-induced glomerular damage. A constitutive nitric oxide synthase (cNOS) has been identified in both human platelets and megakaryoblastic cells. Platelets incubated with cNOS inhibitors demonstrate enhanced aggregation, whereas the cNOS substrate L-arginine inhibits aggregation. Platelets also produce superoxide (O 2 - ) during aggregation. Superoxide and NO- react readily, producing OONO-. It is possible that platelet O 2 - production modifies the bioavailability of NO . for platelets. For this reason, it is relevant to define both NO . and O 2 -release from platelets. The chapter also discusses NO-selective microelectrode for use in a standard platelet aggregometer.
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