期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 281, 期 4, 页码 H1469-H1475出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.281.4.H1469
关键词
nitric oxide; endothelium; smooth muscle
资金
- NHLBI NIH HHS [HL-67930, R01 HL067930, HL-54815, HL-03812] Funding Source: Medline
The myeloperoxidase (MPO)-derived oxidant hypochlorous acid (HOCl) plays a role in tissue injury under inflammatory conditions. The present study tests the hypothesis that HOCl decreases nitric oxide (NO) bioavailability in the vasculature of Sprague-Dawley rats. Aortic ring segments were pretreated with HOCl (1-50 muM) followed by extensive washing. Endothelium-dependent relaxation was then assessed by cumulative addition of acetylcholine (ACh) or the calcium ionophore A23187. HOCl treatment significantly impaired both ACh- and A23187-mediated relaxation. In contrast, endothelium-independent relaxation induced by sodium nitroprusside was unaffected. The inhibitory effect of HOCl on ACh-induced relaxation was reversed by exposure of ring segments to L-arginine but not D-arginine. In cellular studies, HOCl did not alter endothelial NO synthase (NOS III) protein or activity, but inhibited formation of the NO metabolites nitrate (NO3-) and nitrite (NO2-). The reduction in total NO metabolite production in bovine aortic endothelial cells was also reversed by addition Of L-arginine. These data suggest that HOCl induces endothelial dysfunction via modification of L-arginine.
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