Blood platelets relaxing factor

The Relaxing Factor of the Blood Platelets—a Natural Inhibitor of Thrombosthenin Activities... 

Kiardwaj R, Page CP, M GR, Mcx>re PK (1988) Endothelium-derived relaxing factor inhibits platelet aggregation inhuman whole blood in vitro and in the rat in vivo Eur J Pharmacol 157 83-91. 

Houston DS, Robinson P, Gerrard JM (1990) Inhibition of intravascular platelet aggregation by endothelium-derived relaxing factor revo-sal by red blood cells. Blood 76 953-958. 

The nitrates act by releasing nitric oxide, which relaxes vascular smooth muscle. The discovery that endothelium-derived relaxing factor (EDRF) is nitric oxide (1) stimulated new interest in these drugs, as nitric oxide not only controls local vessel wall tension in response to shear stress, but also plays a role in regulating the interaction of platelets with blood vessel walls. The release of nitric oxide from the walls of atheromatous arteries is reduced, because of malfunctioning or absent endothelium. Atheromatous arteries behave differently from healthy arteries, in that these vessels vasoconstrict rather than vasodilate when stimulated by acetylcholine. This impairment of the acetylcholine vasomotor response appears to be related to serum cholesterol concentration (2). 

HDL inhibits monocyte chemotaxis, inhibits the adhesion of monocyte and blood cell to vascular endothelium, inhibits endothelial dysfunction and apoptosis, inhibits LDL oxidation, inhibits complement activation, reduces platelet aggregability and coagulation, inhibits platelet activation, and inhibits factor X activation. HDL helps maintain endothelial integrity, facilitate vascular relaxation, stimulates the proliferation of EC and SMC, stimulates the synthesis of prostacyclin and natriuretic peptide C in EC, stimulates protein C and S activation, and may favor fibrinolysis. These functions are exerted by different components of HDL, this complexity emphasizes that changes in HDL functioning rather than plasma HDL-C levels determine the anti-atherogenicity of therapeutic alterations of HDL metabolism (reviewed in refs. 499 and 500). 

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