Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 291, Issue 5, Pages H2301-H2307Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00349.2006
Keywords
20-hydroxy prostaglandin E-2; 20-carboxy-arachidonic acid; prostaglandins; cerebral vascular tone
Funding
- NHLBI NIH HHS [HL-076684, HL-062984, HL-072845, HL-38901, HL62984, HL-070860] Funding Source: Medline
- NIDDK NIH HHS [DK-038226] Funding Source: Medline
- NIGMS NIH HHS [GM-31278] Funding Source: Medline
- NINDS NIH HHS [NS-24621] Funding Source: Medline
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20-Hydroxyeicosatetraenoic acid (20-HETE), an arachidonic acid (AA) metabolite synthesized by cytochrome P-450 omega-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 U-46619 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-PGE(2), which was as potent as PGE(2) in dilating the basilar artery. 20-HETE also stimulated AA release and PGE(2) and 6-keto-PGF(1 alpha) 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 PGE(2) and 6-keto-PGF(1 alpha) production by the MBEC, but to a lesser extent than 20-HETE. Whereas the conversion of 20-HETE to 20-OH-PGE(2) 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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