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Review
. 2015 Mar;65(3):476-82.
doi: 10.1161/HYPERTENSIONAHA.114.03585. Epub 2015 Jan 12.

Epoxyeicosatrienoic acids, hypertension, and kidney injury

John D Imig  1
Affiliations
Review

Epoxyeicosatrienoic acids, hypertension, and kidney injury

John D Imig. Hypertension. 2015 Mar.
No abstract available

Keywords: chronic renal insufficiency; eicosanoids; hypertension; kidney.

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Figures

Figure 1
Figure 1. Cytochrome P450 epoxygenase metabolites, hypertension, and chronic kidney disease (CKD)
Decreased epoxyeicosatrienoic acids (EETS) contribute to enhanced epithelial sodium channel (ENaC) activity, endothelial dysfunction, and decreased renal blood flow (RBF). These changes in kidney and vascular function contribute to hypertension and CKD.
Figure 2
Figure 2. Therapeutic manipulation of epoxygenase metabolites
Arachidonic acid is converted to epoxyeicosatrienoic acids (EETs) by cytochrome P450 (CYP2C) epoxygenase enzymes. EETs primary metabolic fate is conversion to dihydroxyeicosatrienoic acids (DHETs) by the soluble epoxide hydrolase (sEH) enzyme. EET analogs and sEH inhibitors are two therapeutic approaches being tested to combat hypertension and kidney injury. EET-B has three structural attributes: (1) an acidic or hydrogen bonding replacement (green) for the C(1)-carboxylate to avoid esterification and β-oxidation; (2) a cis-Δ, -olefin or equivalent (red); (3) an epoxide isostere (mimetic) (blue) to obviate sEH metabolism.
See this image and copyright information in PMC

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