Nitric Oxide and Platelet-Mediated Hemostasis

摘要: Nitric oxide (NO·) inhibits platelet function by limiting adhesion and aggregation, as well disaggregating previously aggregated platelets (1–5). Under resting conditions, blood flow stimulates the endothelium to produce NO·, which regulates activity (6–8). NO· activates soluble guanylyl cyclase leading a concomitant increase in production of cyclic guanosine monophosphate (cGMP), principal mediator s effects. As consequence disease states, amount being produced itself may be adversely altered, resulting impairment aggregation function. In this chapter we provide evidence for importance regulating hemostasis, also illustrate role deficiency thrombotic disease.