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1 Anesthesiology, Baylor College of Medicine, Houston, TX, USA
2 Anesthesiology, Baylor College of Medicine, Houston, TX, USA; Medicine (Cardiovascular Sciences), Baylor College of Medicine, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: rbryan{at}bcm.tmc.edu.
We tested the hypotheses that endothelium-derived hyperpolarizing factor (EDHF) in rat middle cerebral arteries (MCAs) involves (a) metabolism of arachidonic acid through the epoxygenase pathway, (b) metabolism of arachidonic acid through the lipoxygenase pathway, or (c) reactive oxygen species. EDHF-mediated dilations were elicited in isolated and pressurized rat MCAs by activation of endothelial P2Y2 receptors with either UTP or ATP. All studies were conducted after inhibition of nitric oxide synthase and cyclooxygenase with L-NAME (10 µM) and indomethacin (10 µM) respectively. Inhibition of epoxygenase with miconazole (30 µM) did not alter EDHF dilations to UTP while the structurally different epoxygenase inhibitor, MS-PPOH (20 or 40 µM), only modestly inhibited EDHF at the highest concentration of UTP. An antagonist of epoxyeicosatrienoic acids, 14,15-EEZE, had no effect on the EDHF dilations to UTP. Chronic inhibition of epoxygenase in the rat with ABT (50mg/kg twice daily for five days) did not alter EDHF dilations. Inhibition of the lipoxygenase pathway with either 10µM baicalein or 10µM NDGA produced no major inhibitory effects on EDHF dilations. The combination of superoxide dismutase (200 units/ml) and catalase (140 units/ml) had no effect on EDHF dilations. Neither tiron (10 mM), a cell permeable scavenger of reactive oxygen species, nor deferoxamine (1 or 10 mM), an iron chelator that blocks the formation of hydroxyl radicals, altered EDHF dilations in the rat MCA. We conclude that EDHF dilations in the rat MCA do not involve the epoxygenase pathway, lipoxygenase pathway, or reactive oxygen species including H2O2.
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