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- W2000589939 abstract "Eicosanoids function as paracrine and autocrine hormones. In endothelial cells, arachidonic acid is metabolized by the cyclooxygenase, lipoxygenase and cytochrome P450 epoxygenase pathways 1 Rosolowsky M. Campbell W.B. Synthesis of hydroxyeicosatetraenoic acids (HETEs) and epoxyeicosatrienoic acids (EETs) by cultured bovine coronary artery endothelial cells. Biochim. Biophys. Acta. 1996; 1299: 267-277 Crossref PubMed Scopus (140) Google Scholar . The epoxygenase pathway leads to the formation of four regioisomeric epoxyeicosatrienoic acids (EETs), 14,15-EET, 11,12-EET, 8,9-EET and 5,6-EET, which are released by endothelial cells in response to receptor agonists such as acetylcholine or bradykinin and act as local, paracrine hormones that relax vascular smooth muscle 2 Campbell W.B. et al. Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors. Circ. Res. 1996; 78: 415-423 Crossref PubMed Scopus (1100) Google Scholar , 3 Fisslthaler B. et al. Cytochrome P450 2C is an EDHF synthase in coronary arteries. Nature. 1999; 401: 493-497 Crossref PubMed Scopus (799) Google Scholar (Fig. 1). EETs cause vasorelaxation by opening large conductance, iberiotoxin-sensitive Ca2+-activated K+ channels (BKCa) in the smooth muscle cell membrane, permitting the efflux of K+; loss of cellular K+ increases the membrane potential or hyperpolarizes the membrane. For these reasons, it is now recognized that EETs represent endothelium-derived hyperpolarizing factors (EDHFs). In many vascular beds EDHFs, like nitric oxide and prostacyclin, regulate vascular tone and mediate the action of receptor agonists. Outside the vasculature, EETs affect ion transport in the kidney, and the release of both insulin and pituitary hormone." @default.
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- W2000589939 date "2000-04-01" @default.
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- W2000589939 title "New role for epoxyeicosatrienoic acids as anti-inflammatory mediators" @default.
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- W2000589939 doi "https://doi.org/10.1016/s0165-6147(00)01472-3" @default.
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