Mechanisms of vasorelaxation induced by eicosapentaenoic acid (20:5n‐3) in WKY rat aorta

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Abstract
The vasorelaxant activity of eicosapentaenoic acid (EPA, 20:5n‐3), the omega‐3 polyunsaturated fatty acid, was investigated in isolated Wistar Kyoto (WKY) rat aortae by measuring isometric tension. Eicosapentaenoic acid (1–100 μM) relaxed rat aortae contracted with high K+ (80 mM) or noradrenaline (NA, 1 μM) in a concentration‐dependent manner. Contractions induced by Bay K 8644 or increasing concentrations of calcium were unaffected by EPA. The relaxant effect of EPA (3–100 μM) was significantly inhibited by indomethacin (10 μM), the cyclo‐oxygenase inhibitor, but not by the nitric oxide (NO) synthesis inhibitor, Nω‐nitro‐L‐arginine methyl ester hydrochloride (L‐NAME, 100 μM). Removal of the endothelium did not alter EPA‐induced relaxations. In Ca2+‐free, EGTA 2 mM solution, EPA (10–30 μM significantly inhibited NA‐sustained contractions. Incubation with EPA (5, 10 μM) diminished both NA‐induced (1 μM) phasic and sustained contractions. The vasorelaxant effects of EPA (30 μM) on NA‐induced (1 μM) contractions were significantly inhibited by the K+ channel blocker, glibenclamide (10 μM), but not tetraethylammonium (1 mM). Moreover, indomethacin and glibenclamide combined significantly inhibited EPA‐induced (1–100 μM) responses. These results indicate EPA exerts its endothelium‐independent vasorelaxant effects in WKY rat aortae through production of prostanoids which activate K+ATP channels. Inhibition of Ca2+ mobilization from intracellular pools and influx through the non‐L‐type, but not the L‐type, Ca2+ channel are also possible mechanisms action of EPA's. British Journal of Pharmacology (2000) 131, 1793–1799; doi:10.1038/sj.bjp.0703754

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