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Mediation of H2O2-induced vascular relaxation by endothelium-derived relaxing factor

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Abstract

We investigated the effects of H2O2 generated by glucose (G) and glucose oxidase (GO) on the isolated rabbit aorta suspended in Krebs-Ringer solution. H2O2 produced contraction in small concentration and relaxation followed by contraction in large concentration. Contraction produced by large concentration was smaller than that produced by small concentration of H2O2. Relaxation was prevented by deendothelialization or NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis. These results suggest that H2O2 in large concentrations produces relaxation followed by contraction, and that the relaxation is endothelium-dependent and is mediated by nitric oxide, an endothelium-derived relaxing factor.

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Authors and Affiliations

  1. Department of Physiology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, S7N 5E5, Saskatoon, Saskatchewan, Canada

    Lalita Bharadwaj & Kailash Prasad

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  1. Lalita Bharadwaj
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  2. Kailash Prasad
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Bharadwaj, L., Prasad, K. Mediation of H2O2-induced vascular relaxation by endothelium-derived relaxing factor. Mol Cell Biochem 149, 267–270 (1995). https://doi.org/10.1007/BF01076587

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