Journal
VASCULAR PHARMACOLOGY
Volume 43, Issue 2, Pages 128-138Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.vph.2005.06.001
Keywords
hydrogen peroxide; rat aorta; arachidonic acid pathway; potassium channels; necrosis cell death
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Four main vascular effects of hydrogen peroxide (H2O2) were studied in intact and rubbed aortic rings from WKY rats. In rings partially precontracted with phenylephrine: 1-30 mu M H2O2 induced an increase of tone, 100 mu M H2O2 produced a transient contraction followed by a fast-developing endothelium-in dependent relaxation, and 0.3 mM H2O2 induced a fast-developing relaxation followed by a slow-developing endothelium-in dependent relaxation. Superoxide dismutase (SOD) or dimethyl sulfoxide (DMSO)/manitol did not significantly modify the H2O2 effects, while catalase suppressed them. Indomethacin abolished the increase of tone elicited by H2O2 and revealed a small endothelium-dependent relaxation, which was suppressed by N-G-nitro-L-arginine (L-NA), high K+ or tetraethylammonium (TEA). TEA strongly inhibited the fast-developing relaxation while indomethacin, glybenclamide, 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), cafeic acid or eicosatdynoic acid (ETI) did not affect the relaxation. In rings precontracted with 70 mM KCI, 1-100 mu M H2O2 induced a small increase of tone and 0.3 mM a slow-developing relaxation. Catalase or Fe2+-EDTA/vitamin C suppressed the slow-developing relaxation while deferoxamine did not modify it. In rings partially precontracted with arachidonic acid, 1-30 PM H2O2, induced higher contractile effects than in rings partially precontracted with phenylephrine. H2O2 at 0.3 mM for one hour induced a persistent impairment on the reactivity of the rings and the release of lactate dehydrogenase. In summary, H2O2, produces: (1) contractions mediated by direct activation of cyclooxygenase; 2) endothelium-dependent relaxations related to activation of endothelial K channels and NO synthesis; 3) reversible endothelium-independent relaxations mediated by activation of smooth muscle K+ channels; and 4) irreversible endothelium-independent relaxations related to cellular damage, caused by H2O2 but not by hydroxyl radicals. (c) 2005 Elsevier Inc. All rights reserved.
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