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1 Biochemistry, University of Iowa, Iowa City, Iowa, United States
2 Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City, Iowa, United States
3 Pathology, University of Iowa, 52242, Iowa, United States
4 Biochemistry, University of Texas Southwestern Medical Center, 75390, Texas, United States
5 Department of Medicine, University of Iowa, Iowa City, Iowa, United States
6 Department of Biochemistry, University of Iowa, Iowa City,, Iowa, United States
* To whom correspondence should be addressed. E-mail: xiang-fang{at}uiowa.edu.
20-Hydroxyeicosatetraenoic acid (20-HETE), an arachidonic acid (AA) metabolite synthesized by cytochrome P450 
-oxidases, is reported to produce vasoconstriction in the cerebral circulation. However, we find that like 14,15-epoxyeicosatrienoic acid (14,15-EET), 20-HETE produces dilation of mouse basilar artery preconstricted with U46619 in vitro. Indomethacin inhibited the vasodilation produced by 20-HETE, but not by 14,15-EET, suggesting a cyclooxygenase (COX)-dependent mechanism. Metabolic studies indicated several mechanisms that may play a role in this process. Mouse brain endothelial cells (MBEC) converted 20-HETE to 20-OH-PGE2, which was as potent as PGE2 in dilating the basilar artery. 20-HETE also stimulated AA release and prostaglandin (PG) E2 (PGE2) and 6-keto-PGF1
production in MBEC. Furthermore, the basilar artery converted 20-HETE to 20-COOH-AA, which also produced COX-dependent dilation of the basilar artery. 20-COOH-AA increased AA release and PGE2 and 6-keto-PGF1|*alpha*| production by the MBEC, but to a lesser extent than 20-HETE. While the conversion of 20-HETE to 20-OH-PGE2 and production of endogenous prostaglandins probably are primarily responsible for vasodilation, the production of 20-COOH-AA also may contribute to this process.
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