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Am J Physiol Heart Circ Physiol (March 21, 2002). doi:10.1152/ajpheart.00007.2002
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Articles in PresS, published online ahead of print March 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00007.2002
Submitted on January 8, 2002
Accepted on March 8, 2002

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

Zsombor Lacza1*, Michelle Puskar2, Bela Kis2, James V. Perciaccante2, Allison W. Miller2, and David W. Busija2

1 Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
2 Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA

* To whom correspondence should be addressed. E-mail: zlacza{at}wfubmc.edu.

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 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 P450 antagonist miconazole (20 µmol/L), the lipoxygenase inhibitors baicalein (10 µmol/L) and CDC (1 µmol/L) failed to reduce the BK induced dilation. However, the H2O2 scavenger catalase (400 U/ml) abolished the response (from 54±11 µm to 0±2 µm, p<0.01). The KATP channel inhibitor glibenclamide (10 µmol/L) had a similar effect as well (from 54±11 µm to 16±5 µm, p<0.05). Coapplication of the KCa 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-NO, non-prostanoid dependent vasorelaxation to BK in the piglet pial vasculature. The response is mediated via BK2 receptors and the opening of KATP-channels.




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