Why the study?
Does endothelium-derived relaxing factor reduce platelet adhesion to endothelial cells?
Does endothelium-derived relaxing factor reduce platelet adhesion to endothelial cells?
Endothelium-derived relaxing factor (EDRF) contributes to the nonadhesive properties of the vascular endothelium by reducing platelet adhesion.
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May inform endothelial anti-adhesive mechanisms in animals; leaves open translation to human thrombosis.
The adhesion of thrombin-stimulated human blood platelets to either the endothelial surface of intact bovine aorta or cultured bovine aortic endothelial cells was studied to determine the role of endothelium-derived relaxing factor in the regulation of platelet adhesion. Endothelial cells and platelets were pretreated with indomethacin to prevent the formation of prostaglandins. The adhesion of thrombin-stimulated platelets to endothelial cells was reduced by superoxide dismutase and bradykinin. The inhibitory effect of both drugs was abolished by hemoglobin and was absent in strips of bovine aorta where the endothelial cells had been removed by scraping. It is suggested that the effects of bradykinin are mediated by the release of endothelium-derived relaxing factor, which is protected from destruction by superoxide dismutase, and that endothelium-derived relaxing factor contributes to the nonadhesive properties of the vascular endothelium.
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Sneddon et al. (1988) studied this question.
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