The involvement of ATP in hypoxic vasodilatation was investigated using isolated perfused guinea-pig hearts (Langendorff). Reactive blue 2, a selective P2Y-purinoceptor antagonist, attenuated dilatations due to ATP and hypoxia. Hydroquinone, an agent which destroys endothelium-derived relaxing factor, substantially decreased dilatations due to 2-methylthioATP, a potent P2Y-purinoceptor agonist, and hypoxia, but not to adenosine. ATP may, therefore, have an important role to play in the initiation of hypoxic dilatation which is mediated by the release of endothelium-derived relaxing factor.
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