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in normotensive rats.

EETs are produced by the endothelium and are potent vasodilators. In the kidney, EETs are produced in the proximal tubule and collecting duct where they inhibit sodium and water reabsorption.33 EETs act as endothelium-derived hyperpolarizing factor (EDHF) independent of NO and prostaglandins where they hyperpolarize vascular smooth muscle cells by activating calcium-activated potassium channels.34 The vasodilatory response to bradykinin in afferent arterioles of the rat juxtamedullary vascular preparation depends on cyclooxygenase metabolites and NO with a significant contribution by EETs.35 Decreased EET levels may play a role in the induction of endothelial dysfunction in experimental models of hypertension. In the kidney microvascular expression of epoxygenase enzymes decreases in angiotensin II hypertension.36 Additionally, increased expression of soluble epoxide hydrolase (sEH), the enzyme responsible for EETs degradation has been reported in angiotensin II-infused rats.33 Thus, the deficiency in the renal formation of EETs may contribute to the development of angiotensin II-dependent forms of hypertension and its associated renal dysfunction. EET and 20-HETE production are altered in experimental and genetic models of hypertension, diabetes, uremia, and pregnancy toxemia, suggesting that the CYP450 metabolites of arachidonic acid contribute to the changes in renal function and vascular tone associated with hypertension and diabetes. However, the contribution of these CYP450 metabolites to renal dysfunction and end-stage renal disease remains largely unexplored.

Arachidonic acid

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