Prostacyclin (PGX) is the endogenous metabolite responsible for relaxation of coronary arteries induced by arachindonic acid

Abstract

The actions of prostacyclin (PGX) and several other derivatives of arachidonic acid were examined on spiral-strips of bovine coronary artery. The strips were contracted by PGE2 and thromboxane A2. Although PGH2 usually cause a transient contraction followed by a relaxation, a few strips were only contracted whilst others were only relaxed. Prostacyclin invariably relaxed coronary artery strips. Sodium arachidonate usually relaxed the strips but occasionally had no effect. Indomethacin increased the resting tone and abolished or substantially reduced the relaxation induced by sodium arachidonate. 15-hydroperoxy arachidonic acid (15-HPAA), a specific inhibitor of prostacyclin synthetase, also increased the resting tone, abolished the effects of sodium arachidonate and the relaxation component of the PGH2 response, but did not greatly modify the relaxation induced by exogenous prostacyclin. These results strongly suggest that prostacyclin mediates the relaxation induced by arachidonic acid in bovine coronary artery strips. As PGH2 is avidly converted into prostacyclin by the vascular tissue of several species including man, prostacyclin is probably involved in the local regulation of the coronary vascular bed.