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Am J Physiol Heart Circ Physiol 283: H406-H411, 2002. First published March 21, 2002; doi:10.1152/ajpheart.00007.2002
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Vol. 283, Issue 1, H406-H411, July 2002

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

Zsombor Lacza1,2, Michelle Puskar1, Béla Kis1, James V. Perciaccante1, Allison W. Miller1, and David W. Busija1

1 Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157; and 2 Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, H1082 Budapest, Hungary

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 Nomega -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-alpha -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.

endothelium-derived hyperpolarizing factor; cerebral circulation; closed cranial window


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