Objective. To evaluate the impact of oxidative stress on vascular reactivity to vasoconstrictors and on nitric oxide (NO) bioavailability in saphenous vein (SV) graft with endothelial dysfunction from hypertensive patients (HT). Methods. Endothelial function, vascular reactivity, oxidative state, nitrites and NO release were studied in isolated SV rings from HT and normotensive patients (NT). Only rings with endothelial dysfunction were used. Results. HT rings presented a hyperreactivity to vasoconstrictors that was reverted by diphenylene iodonium (DPI). In NT, no effect of DPI was obtained, but Nω-nitro arginine methyl ester (L-NAME) increased the contractile response. NO was present in SV rings without endothelial function. Nitrites were higher in NT than in HT (1066.1 ± 86.3？pmol/mg; versus 487.8 ± 51.6; ; ) and inhibited by nNOS inhibitor. L-arginine reversed this effect. Antioxidant agents increased nitrites and NO contents only in HT. The anti-nNOS-stained area by immunohistochemistry was higher in NT than HT. HT showed an elevation of oxidative state. Conclusions. Extraendothelial NO counter-regulates contractility in SV. However, this action could be altered in hypertensive situations by an increased oxidative stress or a decreased ability of nNOS to produce NO. Further studies should be performed to evaluate the implication of these results in graft patency rates. 1. Introduction In coronary artery bypass grafting surgery (CABGS), the vessels that must be used are internal mammary arteries (IMA) and saphenous veins (SV); however, SVs present a greater risk of occlusion [1]. Nitric oxide (NO) could be involved in the improvement of SV graft patency rates [2, 3] since NO plays a pivotal role in vascular homeostasis [4–6]. Three isoforms of NO synthase (NOS) exist: neural (nNOS), inducible (iNOS), and endothelial (eNOS) [7]. Although nNOS was first described in neurons, it is also present in vascular smooth muscle cell (VSMC) [8]. We have shown in IMA that extraendothelial NO is released from nNOS present in VSMC [9, 10]. Oxidative stress plays a role in NO bioavailability [11]. Some studies have reported that superoxide ( ) contributes to the development of hypertension [12, 13]. In experimental hypertension, Li et al. [14] have found elevated levels in veins, suggesting that NADPH oxidase activity induces hyperreactivity to vasoconstrictors. In agreement with these data, we have observed that enhanced NADPH oxidase activity drives production in genetically hypertensive rats [15]. In human IMA, we found that extraendothelial NO counter-regulates
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