Nitric oxide functions as an inhibitor of platelet adhesion under flow conditions.

Abstract

These results demonstrate that NO is a potent inhibitor of platelet adhesion under flow conditions and thereby contributes to the regulatory role of vascular endothelial cells on platelet-vessel wall interaction.

Catalytic consumption of nitric oxide by 12/15- lipoxygenase: Inhibition of monocyte soluble guanylate cyclase activation

“…Under basal conditions, ⅐ NO plays a central role in maintaining vascular homeostasis (56)(57)(58)(59). Thus, stimulation of ⅐ NO consumption by monocytes will contribute to proatherogenic conditions by increasing leukocyte adhesion and margination.…”

Endothelial cell functions

“…Both synergistically increase cAMP content in platelets, hence preventing their aggregation (de Graaf et al, 1992). PGI 2 and NO are constitutively released by endothelial cells but their synthesis is increased in response to a similar range of agonists, notably molecules involved in the coagulation process (e.g., bradykinine and thrombin) or secreted by aggregating platelets (e.g., ATP) and thus serve to limit the intravascular extent of forming thrombi.…”

Effects of l -Arginine on Atherogenesis and Endothelial Dysfunction due to Secondhand Smoke

“…Many of these functions are mediated through the nitric oxide (NO) pathway. Endothelial NO is an important factor that contributes to resting artery tone 8 -10 and possesses antiplatelet 11,12 and antiatherogenic properties that preserve normal arterial structure. 13,14 Although the relationship of endothelial dysfunction to clinical vascular disease is not completely understood, endothelial dysfunction may exist as a pathological state preceding the development of overt atherosclerosis 15 and may contribute to the pathogenesis of acute ischemic syndromes in the development of advanced atherosclerosis.…”