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Cardiovascular-Renal Mechanisms in Health and Disease

Hydrogen peroxide mediates a transient vasorelaxation with tempol during oxidative stress

Cardiovascular Kidney Hypertension Institute and Division of Nephrology and Hypertension, Georgetown University, Washington, District of Columbia

Submitted 6 September 2006 ; accepted in final form 17 July 2007

Tempol catalyzes the formation of H₂O₂ from superoxide and relaxes blood vessels. We tested the hypothesis that the generation of H₂O₂ by tempol in vascular smooth muscle cells during oxidative stress contributes to the vasorelaxation. Tempol and nitroblue tetrazolium (NBT) both metabolize superoxide in vascular smooth muscle cells, but only tempol generates H₂O₂. Rat pressurized mesenteric arteries were exposed for 20 min to the thromboxane-prostanoid receptor agonist, U-46619, or norepinephrine. During U-46619, tempol caused a transient dilation (22 ± 2%), whereas NBT was ineffective (2 ± 1%), and neither dilated vessels constricted with norepinephrine, which does not cause vascular oxidative stress. Neither endothelium removal nor blockade of K⁺ channels with 40 mM KCl affected the tempol-induced dilation, but catalase blunted the tempol dilation by 53 ± 7%. Tempol, but not NBT, increased H₂O₂ in rat mesenteric vessels detected with dichlorofluorescein. To test physiological relevance in vivo, topical application of tempol caused a transient dilation (184 ± 20%) of mouse cremaster arterioles exposed to angiotensin II for 30 min, which was not seen with NBT (9 ± 4%). The vasodilation to tempol was reduced by 68 ± 6% by catalase. We conclude that the transient relaxation of blood vessels by tempol after prolonged exposure to U-46619 or angiotensin II is mediated in part via production of H₂O₂ and is largely independent of the endothelium and potassium channels.

superoxide dismutase; hypertension; angiotensin II; thromboxane

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