Background: Previous studies suggest that psychological stress contribute to atherogenesis, but the mechanism is not well known yet. Stress can induce inflammation of peripheral organs, and inflammation plays a key role in atherogenesis. Therefore inflammation may importantly mediate between stress and atherosclerosis. We studied to assess the effect of stress on vascular pathophysiology. Methods: Male SD rats (8 wk,n=4 for each group) subjected to immobilization stress (2 hr/d) using a restrainer for either 1 wk (IS1) or 2 wk (IS2), or no stress (control). Superior mesenteric arteries and abdominal aortae were used for the assay of acetylcholine (Ach) or nitroprusside(NP) induced vasorelaxation using isometric force displacement transducer and of pathological study, respectively. Expression of inflammatory mediators were assessed by immunohistochemical staining, real time PCR or Western blot. Measurement of plasma nitric oxide metabolite (Nox: nitrate and nitrite) and malondialdehyde (MDA) was carried out at using HPLC. Results: Ach, but not NP, induced vasorelaxation was significantly decreased in IS2, but not in IS1, compared with control. Expression of ICAM-1, VCAM-1, and IL-1b were enhanced in the endothelium of IS2 compared with control. Plasma NOx ���after stress/baseline ratio���was decreased in IS2 compared with control group(0.93 vs 1.53,p<0.05), whereas MDA was not different between two groups. Conclusions: Psychological stress induced endothelial inflammation and endothelial dysfunction in association with inhibition of nitric oxide.