Arachidonic acid (AA, C20 : 4, ω-6) and eicosapentanoic acid (EPA,C20: 5, ω-3), which are polyunsaturated fatty acids forming eicosanoids, were tested for their effects on blood pressure in Wistar rats and SHR. AA is the most important precursor for the biosynthesis of eicosanoids which include the prostaglandins, prostacyclin (PGI₂), thromboxane A₂ (TXA₂) and the leukotriens. TXA₂ is a potent vasoconstrictor and a powerful inducer of platelet aggregation causing myocardial infarction and hypertention. In contrast, PGI₂ induces vasodilation and inhibits platelet aggregation. In this study, AA markedly increased blood pressure, but its effect was antagonized by both EPA, a structural analog of AA, and dazmegrel, a TX synthetase inhibitor. Also, AA enhanced the antihypertensive effects of hydralazine and captopril, and EPA reduced TXA₂ production. These results indicate that the hypotensive effects of EPA might be closely related to the decrease in TXA-2 biosynthesis due to competitive inhibition by structural similarity of the EPA to the AA, the precursor of TXA₂.