An altered vascular reactivity is an important manifestation of the hemodynamic and renal dysfunction during liver cirrhosis. Oxidative stress-derived substances and nitric oxide (NO) have been shown to be involved in those alterations. In fact, both can affect vascular contractile function, directly or by influencing intracellular signaling pathways. Nevertheless, it is unknown whether oxidative stress contributes to the impaired systemic and renal vascular reactivity observed in cirrhosis. To test this, we evaluated the effect of vitamin E supplementation (5000 IU/kg diet) on the vasoconstrictor and vasodilator responses of isolated perfused kidneys and aortic rings of rats with cirrhosis induced by bile duct ligation (BDL), and on the expression of renal and aortic p-ERK1/2 (phospho-Extracellular Regulated Kinase 1/2). BDL induced a blunted renal vascular response to phenylephrine and acetylcholine while BDL aortic rings responded less to phenylephrine but normally to acetylcholine. Cirrhotic rats had higher levels of oxidative stress-derived substances (measured as TBARS) and NO (measured as urinary nitrites excretion) than controls. Vitamin E supplementation normalized the renal hyporesponse to phenylephrine and acetylcholine in BDL, although failed to modify it in aortic rings. Furthermore, vitamin E decreased levels of TBARS, increased levels of NO, and normalized the increased kidney expression of p-ERK1/2 of the BDL rats. In conclusion, BDL rats showed a blunted vascular reactivity to phenylephrine and acetylcholine, more pronounced in the kidney and reversed by vitamin E pre-treatment, suggesting a role for oxidative stress in those abnormalities.