Endothelial dysfunction is induced by proinflammatory oxidant hypochlorous acid

C. Zhang, R. Pate, J. P. Eiserich, F. Zhou, S. Kelpke, W. Ma, D. A. Parks, V. Darley-Usmar, C. R. White

Research output: Contribution to journalArticlepeer-review

61 Scopus citations


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 μM) 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4 50-4
StatePublished - 2001
Externally publishedYes


  • Endothelium
  • Nitric oxide
  • Smooth muscle

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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