H2O2 and tert-butylhydroperoxide (tBHP) induce oxidative stress affecting arterial contraction. We would like to know the effects of peroxide on endothelium in mice aorta. To assess the contractile response to oxidative stress, the specimen obtained from standard mice were exposed to H2O2 and tBHP together with KCl-enriched solution (30mM), contractions were determined. The effects of L-NAME (50mM), ACh, indomethacin (200mM) and endothelial denudation were evaluated. Additionally, free radical generation induced by H2O2 and tBHP was detected by luminol-enhanced chemiluminescence. H2O2 and tBHP increased contraction induced by 30mM KCl in a similar dose dependency. L-NAME increased KCl-induced contraction and the effect of tBHP and H2O2. ACh relaxed KCl-induced contraction and the contraction induced by H2O2. Furthermore, L-NAME did not increase KCl-induced contraction in denuded endothelium aorta. Removal of endothelium increased the contraction by tBHP but not that H2O2. In addition, indomethacin abolished H2O2 and tBHP-induced contraction. Finally, H2O2 greatly increased total free radical production, which was strongly decreased by indomethacin. In contrast, tBHP increased the production of total free radical only slightly. H2O2 and tBHP induced oxidant stress by different mechanisms to increase arterial contraction. This effect was modulated by the endothelium function. Endothelial nitric oxide has a protective role on the contraction induced by tBHP.