Abstract
In their recent article ‘Vascular tolerance to nitroglycerin (GTN) in ascorbate deficiency' Wölkart et al. demonstrated an impaired vasodilator potency of GTN in ascorbate-deficient guinea pigs.1 The authors also conclude from the lack of an effect of polyethylene-glycolated superoxide dismutase (PEG-SOD) and catalase (PEG-catalase), that the impairment of GTN vasodilator potency induced by ascorbate deficiency is not mediated by induction of oxidative stress (their Figure 3). Although these data are interesting, especially in the context of the previous literature suggesting a role of oxidative stress in the development of nitrate tolerance, we believe that several points deserve further discussion.