The Role of NADPH Oxidase on L-NAME-Induced Leukocyte-Endothelial Interactions in Rat Mesenteric Postcapillary Venules

摘要

Chronic inflammation can lead to endothelial dysfunction causing further inflammation, setting up a vicious cycle. Inflammatory responses are thought to underlie the pathogenesis of many vascular-related diseases and are characterized by decreased production of endothelium-derived nitric oxide (NO) by endothelial NO synthase (eNOS) and increased reactive oxygen species (ROS) particularly, superoxide (SO) {1,2]. The inflammatory responses involve increased leukocyte-endothelial interactions and activation of NADPH oxidase causing ROS release. We hypothesized that the selective NADPH oxidase inhibitors, apocynin (mol.wt.=166 g/mol, Sigma Chemicals) [3] and gp91 ds-tat (RKKRRQRRR-CSTRIRRQL-amide, mol.wt.=2452 g/mol, Genemed Synthesis, San Antonio, TX) [4], will attenuate leukocyte-endothelial interactions induced by inhibition of eNOS activity via N~G-nitro-L-arginine-methyl-ester (L-NAME).