Platelet adhesion to human vascular endothelium is modulated by constitutive and cytokine induced nitric oxide

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Abstract
Objective: The aim was to study whether basal or cytokine stimulated generation of nitric oxide (NO) modulates platelet adhesion to human umbilical vein endothelial cells (HUVEC). Methods: The adhesion of 111In labelled human platelets to transfected HUVEC (SGHEC-7) was measured either alone or after incubation of SGHEC-7 cells for 18 h with interleukin-1β (IL-1β) and/or tumour necrosis factor a (TNFα). The activity of NO synthase in these cells was measured by formation of citrulline. The effects of dexamethasone (0.3 μM) and NG-monomethyl-L-arginine (L-NMMA, 100 μM) on these two variables were determined. Results: Stimulation of SGHEC-7 cells with IL-1β or TNFα (each at 1-30 ng·ml−1) caused them to express the inducible NO synthase, an effect that was prevented by dexamethasone. Platelet adhesion to unstimulated SGHEC-7 cells was Conclusions: Inhibition of NO synthesis by L-NMMA potentiates platelet adhesion to unstimulated SGHEC-7 cells, showing that basally released NO regulates platelet adhesion. Stimulation of SGHEC-7 cells by cytokines increases their adhesive properties but at the same time causes them to express the inducible NO synthase. Nitric oxide generated by this enzyme contributes to the modulation of the adhesive properties of the endothelial cells. Thus both constitutive and inducible NO synthases modulate endothelial cell thrombogenicity. Cardiovascular Research 1993;27:1380-1382

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