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CARDIOVASCULAR

Increased Superoxide Anion Production by Interleukin-1 Impairs Nitric Oxide-Mediated Relaxation in Resistance Arteries

Departament de Farmacologia, Terapèutica i Toxicología (F.J.-A., A.M.B., E.V.), Unitat de Bioestadística (J.G.), Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain; Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas, Institut d'Investigacions Biomèdiques August Pi Sunyer (A.M.P.), Barcelona, Spain; and Departamento de Farmacología (M.S., A.M.B.), Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain

The present study was designed to analyze the effect of long-term incubation with interleukin-1 (IL-1) on endothelium-dependent relaxation in rat mesenteric resistance arteries. Vessels were incubated in culture medium with or without IL-1 (10 ng/ml, 14 h). Changes in lumen diameter were recorded in a pressure myograph. Protein expression, nitrite, and superoxide anion () production were evaluated by either Western blot or immunofluorescence, Griess reaction, and ethidium fluorescence, respectively. IL-1 impaired acetylcholine (ACh) and sodium nitroprusside (SNP) vasodilation and increased nitrite and production and inducible nitric-oxide synthase (iNOS), xanthine oxidase, and p22^phox expression. However, neither endothelial nitric-oxide synthase (NOS) nor soluble guanylate cyclase protein expression were affected by IL-1 treatment. Polyethylene glycol superoxide dismutase partially reversed the impairment of ACh relaxation and abolished the production observed in IL-1-treated arteries. The impairment of ACh relaxation induced by IL-1 was also partially reversed by the xanthine oxidase inhibitor allopurinol (1 mM) but not by either the NADPH oxidase inhibitor apocynin (0.3 mM) or the inducible NOS inhibitor N-3-aminomethylbenzylacetamidine (1 µM). However, all these inhibitors improved the impaired SNP response. The results of the present study demonstrate that long-term incubation with IL-1 induces an impairment of the nitric oxide-mediated relaxation in mesenteric resistance arteries through the production of , mainly from xanthine oxidase.

Address correspondence to: Prof. Elisabet Vila, Departament de Farmacologia, Terapèutica i Toxicologia, Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona; 08193 Bellaterra, Spain. E-mail: elisabet.vila{at}uab.es

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