Role of nitric oxide in biological effects of vascular endothelial growth factor

Abstract

To evaluate the role of nitric oxide in the biological effects of vascular endothelial growth factor (VEGF) and the possible mechanism of VEGF, the in vitro cultured vascular endothelial cells of rabbit aorta were divided into control group, VEGF-treated group and VEGF+ N-nitro-L-arginine methyl ester (L-NAME)-treated group. The absorbance (A) value of vascular endothelial cells and the levels of prostaglandin (PGI₂), endothelin-1 (ET-1) and von Willebrand factor (vWF) in the supernatant were observed by water-soluble tetrazolium salt assay, radioimmunoassay and enzyme-linked immunosorbent assay. The A values and PGI₂ in VEGF-treated group and VEGF+L-NAME-treated group were higher than those in control group (P<0.05 and P<0.01). The ET-1 and vWF were significantly decreased in VEGF-treated group and VEGF+L-NAME-treated group compared with the control (P<0.05 and P<0.01). These results indicate that VEGF could promote the proliferation and secretion of PGI₂ and inhibit the secretion of ET-1 and vWF in vascular endothelial cells and that L-NAME could inhibit the effect of VEGF partially. Nitric oxide is an important mediator in the process of stimulating proliferation and regulating secretion of vascular endothelial cells by VEGF.

Keywords

vascular endothelial growth factor / nitric oxide / N-nitro-L-arginine methyl ester / vascular endothelial cells