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1 Biochemistry, University of Iowa, Iowa City, IA, USA
2 Internal Medicine, University of Iowa, Iowa City, IA, USA
3 Entomology, University of California, Davis, CA, USA
4 Biochemistry, University of Iowa, Iowa City, IA, USA; Internal Medicine, University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: xiang-fang{at}uiowa.edu.
We investigated the effects of soluble epoxide hydrolase (sEH) inhibition on epoxyeicosatrienoic acid (EET) metabolism in intact human blood vessels, including saphenous vein (HSV), coronary artery (HCA), and aorta (HA). When HSV segments were perfused with 2 µmol/L [3H]14,15-EET for 4 h, > 60% of radioactivity in the perfusion medium was converted to 14,15-dihydroxyeicosatrienoic acid (DHET). Similar results were obtained with endothelium-denuded vessels. 14,15-DHET was released from both the luminal and adventitial surfaces of the HSV. When HSV were incubated with [3H]14,15-EET under static (no flow) conditions, formation of 14,15-DHET was detected within 15 min and was inhibited by the selective sEH inhibitors N,N'-dicyclohexyl urea and N-cyclohexyl-N'-dodecanoic acid urea (CUDA). Similarly, CUDA inhibited the conversion of [3H]11,12-EET to 11,12-DHET by HSV. sEH inhibition enhanced the uptake of [3H]14,15-EET and facilitated the formation of 10,11-epoxy-16:2, a 
-oxidation product. HCA and HA converted [3H]14,15-EET to DHET, and this also was inhibited by CUDA. These findings in intact human blood vessels indicate that conversion to DHET is the predominant pathway for 11,12- and 14,15-EET metabolism and that sEH inhibition can modulate EET metabolism in the vascular tissue.
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