Hydrogen peroxide acts as an EDHF in the piglet pial vasculature in response to bradykinin

Zsombor Lacza, Michelle Puskar, Béla Kis, James V. Perciaccante, Allison W. Miller, David W. Busija

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We investigated the mechanism of EDHF-mediated dilation to bradykinin (BK) in piglet pial arteries. Topically applied BK (3 μmol/l) induced vasodilation (62 ± 12%) after the administration of Nω-nitro-L-arginine methyl ester (L-NAME) and indomethacin, which was inhibited by endothelial impairment or by the BK2 receptor antagonist HOE-140 (0.3 μmol/l). Western blotting showed the presence of BK2 receptors in brain cortex and pial vascular tissue samples. The cytochrome P-450 antagonist miconazole (20 μmol/l) and the lipoxygenase inhibitors baicalein (10 μmol/l) and cinnamyl-3,4-dyhydroxy-α-cyanocinnamate (1 μmol/l) failed to reduce the BK-induced dilation. However, the H2O2 scavenger catalase (400 U/ml) abolished the response (from 54 ± 11 to 0 ± 2 μm; P < 0.01). The ATP-dependent K+ (KATP) channel inhibitor glibenclamide (10 μmol/l) had a similar effect as well (from 54 ± 11 to 16 ± 5 μm; P < 0.05). Coapplication of the Ca2+-dependent K+ channel inhibitors charybdotoxin (0.1 μmol/l) and apamin (0.5 μmol/l) failed to reduce the response. We conclude that H2O2 mediates the non-nitric oxide-, non-prostanoid-dependent vasorelaxation to BK in the piglet pial vasculature. The response is mediated via BK2 receptors and the opening of KATP channels.

Original languageEnglish
Pages (from-to)H406-H411
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 52-1
Publication statusPublished - Jul 10 2002



  • Cerebral circulation
  • Closed cranial window
  • Endothelium-derived hyperpolarizing factor

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Lacza, Z., Puskar, M., Kis, B., Perciaccante, J. V., Miller, A. W., & Busija, D. W. (2002). Hydrogen peroxide acts as an EDHF in the piglet pial vasculature in response to bradykinin. American Journal of Physiology - Heart and Circulatory Physiology, 283(1 52-1), H406-H411.