Recovery by ascorbate of impaired nitric oxide‐dependent relaxation resulting from oxidant stress in rat aorta

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Abstract
1 In this study we investigated the ability of ascorbate to protect nitric oxide from destruction by superoxide anion. 2 Ascorbate produced concentration‐dependent relaxation of rings of rat aorta, comprising two components: the first, seen at 1–300 μM, reached a maximum of 45.3±2.8%, and was abolished by endothelial removal or treatment with L‐NAME (100 μM), demonstrating involvement of nitric oxide. The second occurred at concentrations of 1 mM and above and was associated with falls in the pH of the bathing fluid. 3 Pretreatment with ascorbate at concentrations up to 3 mM had no effect on the relaxation to acetylcholine (10 nM–10 μM) on endothelium‐containing rings or adenosine (0.1 μM–3 mM) on endothelium‐denuded rings. 4 An oxidant stress was applied to aortic rings, comprising inhibition of endogenous Cu/Zn superoxide dismutase by diethyldithiocarbamate (0.1 mM) followed by generation of superoxide anion by hypoxanthine (0.1 mM/xanthine oxidase (16 u ml−1). This reduced maximal acetylcholine‐induced relaxation from 96.7±1.3% to 42.4±3.5% (PBritish Journal of Pharmacology (1998) 125, 782–786; doi:10.1038/sj.bjp.0702120

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