Hydrogen peroxide is an endothelium-derived hyperpolarizing factor in human mesenteric arteries

Tetsuya Matoba, Hiroaki Shimokawa, Hiroshi Kubota, Keiko Morikawa, Takako Fujiki, Ikuko Kunihiro, Yasushi Mukai, Yoji Hirakawa, Akira Takeshita

Research output: Contribution to journalArticlepeer-review

241 Citations (Scopus)


The endothelium plays an important role in maintaining vascular homeostasis by synthesizing and releasing several vasodilating factors, including prostacyclin, nitric oxide, and endothelium-derived hyperpolarizing factor (EDHF). We have recently identified that endothelium-derived hydrogen peroxide (H2O2) is an EDHF in mice. The present study was designed to examine whether this is also the case in humans. Bradykinin elicited endothelium-dependent relaxations and hyperpolarizations in the presence of indomethacin and Nω-nitro-L-arginine, which thus were attributed to EDHF, in human mesenteric arteries. The EDHF-mediated relaxations were significantly inhibited by catalase, an enzyme that specifically decomposes H2O2, whereas catalase did not affect endothelium-independent hyperpolarizations to levcromakalim. Exogenous H2O2 elicited relaxations and hyperpolarizations in endothelium-stripped arteries. Gap junction inhibitor 18α-glycyrrhetinic acid partially inhibited, whereas inhibitors of cytochrome P450 did not affect the EDHF-mediated relaxations. These results indicate that H2O2 is also a primary EDHF in human mesenteric arteries with some contribution of gap junctions.

Original languageEnglish
Pages (from-to)909-913
Number of pages5
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - 2002
Externally publishedYes


  • Bradykinin
  • Catalase
  • Endothelium-derived hyperpolarizing factor
  • Hydrogen peroxide
  • Levcromakalim
  • Membrane potential
  • Nitric oxide
  • Potassium channel
  • Vascular endothelium

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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