Nitric oxide (NO) is released by the endothelium preventing platelet adhesion to the vessel wall. When released by platelets, NO inhibits further recruitment of platelets to a growing thrombus. Modulation of endogenous NO release may be a mechanism by which the thrombotic response can be regulated as suggested by several clinical diseases associated with impaired bioactive NO. Diseases including atrial fibrillation and coronary atherothrombotic disease have been associated with impaired NO release or decrease in NO bioavailability.