The effect of arachidonic- and eicosapentaenoic acid on the synthesis of prostacyclin-like material in human umbilical vasculature.
All cis-5,8,11,14,17 eicosapentaenoic acid (EPA) inhibits platelet aggregation. The mechanisms for this inhibition are not known in detail. One of them might be a competitive inhibition of TXA2 production. Even if rat and human vasculature in pure systems covert EPA to PGI3 with the same properties as PGI2, it is essential to known if EPA influences the conversion of arachidonic acid (AA) to PGI2 in human vasculature. This problem was investigated in human umbilical vascular tissue deprived of substrate for PGI synthesis. After incubation with AA or EPA alone and in combinations, prostacyclin synthesis was measured as PGI2. Prostacyclin production in assays with AA and EPA in combinations in the incubation mixture, was found additive as calculated from assays with pure substrates. Thus, EPA did not influence the conversion of AA to PGI2 but gave obviously rise to additional synthesis of PGI-like material.
D001095:Arachidonic Acids / Q000494:pharmacology*; D001808:Blood Vessels; D004537:Eicosanoic Acids / Q000494:pharmacology*; D015118:Eicosapentaenoic Acid; D011464:Epoprostenol / Q000096:biosynthesis*; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis; D014472:Umbilicus / Q000098:blood supply*
D001095:Arachidonic Acids; D004537:Eicosanoic Acids; D005231:Fatty Acids, Unsaturated; D011453:Prostaglandins; D013931:Thromboxanes; D015118:Eicosapentaenoic Acid; D011464:Epoprostenol