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Adenosine, prostaglandins (PG) and nitric oxide (NO) have all been implicated in hypoxia‐evoked vasodilatation. We investigated whether their actions are interdependent. In anaesthetised rats, the PG synthesis inhibitors diclofenac or indomethacin reduced muscle vasodilatation evoked by systemic hypoxia or adenosine, but not that evoked by iloprost, a stable analogue of prostacyclin (PGI₂), or by an NO donor. After diclofenac, the A₁ receptor agonist CCPA evoked no vasodilatation: we previously showed that A₁, but not A_2A, receptors mediate the hypoxia‐induced muscle vasodilatation. Further, in freshly excised rat aorta, adenosine evoked a release of NO, detected with an NO‐sensitive electrode, that was abolished by NO synthesis inhibition, or endothelium removal, and reduced by ≈50 % by the A₁ antagonist DPCPX, the remainder being attenuated by the A_2A antagonist ZM241385. Diclofenac reduced …