As increasing evidence suggest that oxidative stress plays an important role in the developing angiopathy in diabetes, we studied the effects of taurine, a free radical scavenger, on diabetesinduced angiopathy in the rat aorta. Six-week-old male Wistar rats were randomly divided into three groups; control group (Cont), diabetes group (DM) and diabetes group treated with taurine for four weeks, 500 mg/kg/day, intraperitoneally (i.p.) (DM+T). Diabetes was induced by streptozotocin (50 mg/kg i.p.). Four weeks after the induction of diabetes, serum glucose and malondialdehyde concentrations were measured. Additionally, organ bath studies and real-time PCR on muscarinic M 3 receptor and eNOS were performed. Although taurine treatment failed to decrease serum glucose levels, the increased serum malondialdehyde levels in diabetic rats were significantly decreased after taurine treatment. Norepinephrine-induced hyper-contractility as well as acetylcholine-induced, endothelium-dependent hypo-relaxation in diabetes were significantly prevented after taurine treatment. The differences in the expressions of muscarinic M 3 receptor mRNAs were statistically non-significant between groups. Moreover, diabetes-induced up-regulation of eNOS mRNAs was slightly prevented after taurine treatment. These data suggest that taurine acts beneficially against the diabetes-induced vascular dysfunction. Its potential action as a radical scavenger ameliorates the vascular disorders in diabetes.Vascular disease is a prominent sequela of both type-1 and type-2 diabetes (7). Cardiovascular disease alters vascular responsiveness to several vasoconstrictors and vasodilators and is a major factor underlying the development of this disease (21). Most of the complications in diabetes are caused by the increased serum glucose and the increased generation of oxygen-derived free radicals, which lead to endothelium dysfunction and neuropathy. Although strict glycemic control delays the onset and slows down the progression of diabetic vascular complications (8, 25), this strategy is not successful in all patients. It has been demonstrated that there are functional changes in various smooth muscle cells in diabetic animals (16). Oxidative stress plays a pivotal role in the development of diabetes complications, both microvascular and cardiovascular. The metabolic abnormalities of diabetes cause mitochondrial superoxide overproduction in endothelial cells of both large and small vessels, as well as in the myocardium. The increased superoxide production causes the activation of five major pathways involved in the pathogenesis of microvascular and cardiovascular damage: polyol pathway flux, increased formation of advanced glycation end products (AGEs), increased expression of the receptor for AGEs and its activating ligands, activation of protein kinase C