Prostacyclin releases endothelium‐derived relaxing factor and potentiates its action in coronary arteries of the pig

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Abstract
1 The possible interactions between prostacyclin and endothelium-derived relaxing factor were examined, in isolated coronary arteries of the pig treated with indomethacin (10−5 m). 2 In organ chamber experiments, prostacyclin caused relaxations, which were potentiated in the presence of the endothelium; the potentiation was abolished by oxyhaemoglobin. 3 In bioassay experiments, prostacyclin caused minimal relaxations of bioassay rings without endothelium; these relaxations were potentiated when the bioassay ring was exposed to basally-released endothelium-derived relaxing factor (interaction between prostacyclin and basal endothelium-derived relaxing factor) and further augmented when the endothelial cells were exposed to the prostanoid (stimulated release of endothelium-derived relaxing factor). The endothelium-dependent, but not the direct effects of prostacyclin were augmented by superoxide dismutase plus catalase and abolished by oxyhaemoglobin. 4 Forskolin, a direct activator of adenylate cyclase, caused relaxations of rings without endothelium, which were augmented by the presence of the endothelium. 5 The relaxations induced by prostacyclin or forskolin also had an endothelium-dependent component in basilar and femoral arteries and in jugular veins of the pig. 6 The endothelium-dependent actions of prostacyclin probably reflect activation of adenylate cyclase.