20-Hydroxyeicosatetraenoic acid is an endothelium-dependent vasoconstrictor in rabbit arteries
References (30)
- et al.
Modulation of erythropoiesis by novel human bone marrow cytochrome P-450-dependent metabolites of arachidonic acid
Blood
(1991) - et al.
Influence of a fibric acid type of hypolipidemic agent on the oxidative metabolism of arachidonic acid by liver microsomal cytochrome P450
Arch. Biochem. Biophys.
(1985) - et al.
Vasoactivity of arachidonic acid epoxides
Eur. J. Pharmacol.
(1987) - et al.
Synthesis of arachidonic acid metabolites produced by purified kidney cortex microsomes cytochrome P450
Tetrahedron Lett.
(1983) - et al.
Cytochrome P450-dependent arachidonic acid metabolism in human kidney
Kidney Int.
(1990) - et al.
Structural identification of cytochrome P450-dependent arachidonate metabolites formed by rabbit medullary thick ascending limb cells
J. Biol. Chem.
(1991) - et al.
Cyclooxygenase dependency of the renovascular actions of cytochrome P450-derived arachidonate metabolites
J. Pharmacol. Exp. Ther.
(1992) - et al.
Cytochrome P450-dependent metabolism of arachidonic acid by microsomes from renal vessels
FASEB J.
(1990) - et al.
Cytochrome P450-linked monooxygenase, involvement in the lamb ductus arteriousus
Am. J. Physiol.
(1984) - et al.
Dexamethasone (Dex) increases renal arachidonic acid metabolism by a non-cyclooxygenase pathway
FASEB J.
(1991)
Concentration of prostaglandin endoperoxide synthase and prostaglandin I2 synthase in the endothelium and smooth muscle of bovine aorta
J. Clin. Invest.
Vasoactivity of 20-hydroxyeicosatetraenoic acid is dependent on metabolism by cyclooxygenase
J. Pharmacol. Exp. Ther.
Effect of cytochrome P450 arachidonate metabolites on ion transport in rabbit kidney loop of Henle
Science
Sites of prostaglandin synthesis in the bovine heart and isolated bovine coronary microvessels
Circ. Res.
Cited by (66)
20-HETE in the regulation of vascular and cardiac function
2018, Pharmacology and TherapeuticsCitation Excerpt :The link between 20-HETE and hypertension was originally documented in studies indicating that depletion and inhibition of CYP4A reduced blood pressure in the SHR (DaSilva et al., 1994; Escalante, Sacerdoti, Davidian, Schwartzman, & McGiff, 1991; Sacerdoti et al., 1989). These and other studies (Su, Kaushal, & Kroetz, 1998; Xu et al., 2002), together with reports that 20-HETE is a vasoconstrictor (Escalante et al., 1993; Laniado-Schwartzman, Falck, Yadagiri, & Escalante, 1989; Ma et al., 1993), suggested that increased 20-HETE synthesis and/or actions contributed to increased blood pressure in SHR and other experimental models of hypertension (Alonso-Galicia, Maier, Greene, Cowley Jr., & Roman, 2002; Moreno, Maier, Hoagland, Yu, & Roman, 2001; Muthalif et al., 2000; Muthalif et al., 2000)(30-33). Other studies substantiated the notion that 20-HETE contributes to the development of hypertension by demonstrating that: (i) the synthesis of and vascular reactivity to 20-HETE are significantly higher in the SHR than in normotensive rats (Imig et al., 1993; F. Zhang et al., 2001), (ii) inhibition of vascular 20-HETE synthesis by CYP4A2 antisense oligonucleotides decreases blood pressure (M. H. Wang et al., 1998; M. H. Wang et al., 2001), (iii) vascular-selective transduction of CYP4A2 cDNA increases vascular 20-HETE synthesis and produces hypertension in SD rats (Inoue, Sodhi, et al., 2009; J. S. Wang et al., 2006), and (iv) administration of a 20-HETE analog prevents the fall in blood pressure in LPS-induced endotoxic shock in rats (Tunctan et al., 2008).
Why and How Drugs Fail
2017, Innovative Approaches in Drug Discovery: Ethnopharmacology, Systems Biology and Holistic TargetingSoluble epoxide hydrolase null mice exhibit female and male differences in regulation of vascular homeostasis
2015, Prostaglandins and Other Lipid MediatorsNS-398 reverses hypotension in endotoxemic rats: Contribution of eicosanoids, NO, and peroxynitrite
2013, Prostaglandins and Other Lipid MediatorsCitation Excerpt :20-HETE is an ω-hydroxylation product of arachidonic acid that is produced by cytochrome P450 (CYP) enzymes, mainly by the CYP4A and CYP4F isoforms in the kidney, heart, liver, brain, lung, and the vasculature [6–8]. In the vasculature, 20-HETE causes vasoconstriction in several vascular beds, including renal, cerebral, aortic, mesenteric, and coronary arteries [9–13]. 20-HETE activates protein kinase C [14–17], MAPK [18–20], Raf/mitogen-activated protein kinase kinase (MEK)/ERK [21], and Rho-kinase [10] pathways, which all contribute to the regulation of vascular tone.
5,14-HEDGE, a 20-HETE mimetic, reverses hypotension and improves survival in a rodent model of septic shock: Contribution of soluble epoxide hydrolase, CYP2C23, MEK1/ERK1/2/IKKβ/IκB-α/NF-κB pathway, and proinflammatory cytokine formation
2013, Prostaglandins and Other Lipid MediatorsCitation Excerpt :20-hydroxyeicosatetraenoic acid (20-HETE) is an ω-hydroxylation product of arachidonic acid (AA) that is produced by cytochrome P450 (CYP) enzymes, mainly by the CYP4A and CYP4F isoforms in the kidney, heart, liver, brain, lung, and vasculature [1–4]. In the vasculature, 20-HETE causes vasoconstriction in several vascular beds, including renal, cerebral, aortic, mesenteric, and coronary arteries [5–9]. Activation of protein kinases, such as mitogen-activated protein kinase (MAPK), MAPK kinase (MEK), and extracellular signal-regulated kinase (ERK) which contribute to the regulation of vascular tone, has been shown to mediate to the vasoconstrictor effect of 20-HETE [10–13].