20-HETE

Short Summary : Vasoconstrictor in renal and cerebral vasculature

Category : Membrane Transporter/Ion Channel|ATPase

Purity : 0.98

CAS Number : 79551-86-3

Formula : C20H32O3

Molecular Weight : 320.47

SMILE : C(CCC=CCC=CCC=CCC=CCCCC(=O)O)CCO

Solubility : Soluble in Ethanol

Storage : Store at -20°C

Description : 20-HETE is a potent vasoconstrictor with EC50 value of < 10 nM [1].20-HETE is a metabolite of arachidonic acid through the cytochrome P450 metabolic pathway. The members of CYP4 gene family producing 20-HETE in humans are predominantly CYP4A11 (in proximal tubules) and CYP4F2 (in human kidney). 20-HETE regulates blood pressure in a complex way. It inhibits the Na+ reabsorption and K+ efflux in medullary TALH and inhibits the activity of Na+-K+-ATPase in proximal tubules. In the microvasculature, 20-HETEsensitizes smooth muscle cells to the constrictor stimuli, promotes the proliferation of endothelial cells and induces the endothelial cell dysfunction. In addition, 20-HETE has the ability to induce proinflammatory changes [2].20-HETE inhibited sodium transport through activating PKC to phosphorylate the serine23 residue in theαsubunit of the Na+-K+-ATPase. In TALH cells, 20-HETE blocked the 70 pS K+ channel localized in the apical membrane. Besides that, 20-HETE was found to be a potent vasoconstrictor through activating the kinase pathways that contribute to the vascular tone regulation including MAPK, PKC, rho kinase and src-type tyrosine kinase [1].In the Dahl salt-sensitive rats, the formation of 20-HETEwas reduced in the kidney, resulted in the elevated loop Cl- reabsorption. Increasing the formation of 20-HETE by fibrates, SOD mimetic or Tempol showed the antihypertensive effects. In the spontaneously hypertensive rats, the production of 20-HETE was elevated in vessel and that subsequently caused the endothelial dysfunction, oxidative stress and elevated vascular reactivity to pressor hormones. Besides that, in mice with CYP4A14 gene knockout, blood pressure was also elevated due to the expression upregulation of the CYP4A12 gene and the subsequently20-HETE production increase [1]. References:[1] Williams JM1, Murphy S, Burke M, Roman RJ. 20-hydroxyeicosatetraeonic acid: a new target for the treatment of hypertension. J Cardiovasc Pharmacol. 2010 Oct;56(4):336-44.[2] Wu CC1, Gupta T, Garcia V, Ding Y, Schwartzman ML. 20-HETE and blood pressure regulation: clinical implications. Cardiol Rev. 2014 Jan-Feb;22(1):1-12.

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