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From the Department of Clinical Pharmacology, Cardiovascular Division, School of Medicine, Kings College London, UK.
Correspondence to Dr Albert Ferro, 3.07 Franklin Wilkins Building, Kings College London, 150 Stamford Street, London SE1 9NH, UK. E-mail albert.ferro{at}kcl.ac.uk
Nitric oxide (NO) exerts important vasodilatory, antiplatelet, antioxidant, antiadhesive, and antiproliferative effects. Although endothelium derived NO has been shown to be of prime importance in cardio- and vasculoprotection, until recently little was known about the role of platelet-derived NO. New evidence suggests that NO synthesized by platelets regulates platelet functions, in particular suppressing platelet activation and intravascular thrombosis. Moreover, platelet NO biosynthesis may be decreased in patients with cardiovascular risk factors or with coronary heart disease, and this may contribute to arterial thrombotic disease in these patients. Here, we review the current state of knowledge as regards the role of platelet-derived NO, both in normal physiology and in cardiovascular disease states, and compare platelet NO signaling and regulation with that in endothelial cells.
Key Words: platelets nitric oxide cardiovascular physiology cardiovascular disease
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