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lüll Role of arachidonic acid lipoxygenase metabolites in the regulation of vascular tone Chawengsub Y; Gauthier KM; Campbell WBAm J Physiol Heart Circ Physiol 2009[Aug]; 297 (2): H495-507Stimulation of vascular endothelial cells with agonists such as acetylcholine (ACh) or bradykinin or with shear stress activates phospholipases and releases arachidonic acid (AA). AA is metabolized by cyclooxygenases, cytochrome P-450s, and lipoxygenases (LOs) to vasoactive products. In some arteries, a substantial component of the vasodilator response is dependent on LO metabolites of AA. Nitric oxide (NO)- and prostaglandin (PG)-independent vasodilatory responses to ACh and AA are reduced by inhibitors of LO and by antisense oligonucleotides specifically against 15-LO-1. Vasoactive 15-LO metabolites derived from the vascular endothelium include 15-hydroxy-11,12-epoxyeicosatrienoic acid (15-H-11,12-HEETA) that is hydrolyzed by soluble epoxide hydrolase to 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA). HEETA and THETA are endothelium-derived hyperpolarizing factors that induce vascular relaxations by activation of smooth muscle apamin-sensitive, calcium-activated, small-conductance K(+) channels causing hyperpolarization. In other arteries, the 12-LO metabolite 12-hydroxyeicosatetraenoic acid is synthesized by the vascular endothelium and relaxes smooth muscle by large-conductance, calcium-activated K(+) channel activation. Thus formation of vasodilator eicosanoids derived from LO pathways contributes to the regulation of vascular tone, local blood flow, and blood pressure.|8,11,14-Eicosatrienoic Acid/*analogs & derivatives/metabolism[MESH]|Animals[MESH]|Arachidonate 12-Lipoxygenase/*metabolism[MESH]|Arachidonate 15-Lipoxygenase/*metabolism[MESH]|Endothelium, Vascular/*enzymology[MESH]|Humans[MESH]|Vasodilation/*physiology[MESH] |