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al o f P hy si ol og y It is generally accepted that adenosine plays a major role in vasodilatation evoked by hypoxia in several different tissues including skeletal muscle, heart and brain (Berne et al. 1983). Indeed, when the actions of adenosine are prevented in these tissues, hypoxia-induced dilatation is greatly reduced or even abolished (Berne et al. 1983; Bryan & Marshall, 1999a; Coney & Marshall, 1998; Nakhostine & Montagne, 1994). However, there is also substantial evidence that hypoxia-induced dilatation is mediated by newly synthesised prostaglandins (PGs): when PG synthesis is blocked hypoxia-induced dilatation is reduced or abolished (Busse et al. 1984; Fredricks et al. 1994b; Messina et al. 1992). This raises the possibility that adenosine- and PG-induced dilatation are synergistic, or that the dilatation induced by one is somehow dependent on the other. The main aim of the present study was to investigate the possible interrelationships between adenosine and PGs more fully, by investigating the vasodilatation evoked in skeletal muscle of the rat by systemic hypoxia. This response we have previously attributed in part to adenosine acting on A1 but not A2A receptors, even though exogenous adenosine produces muscle vasodilatation by stimulating both A1 and A2A receptors (Bryan & Marshall, 1999a). Experiments described herein produced the novel finding that a large part of the hypoxia-induced muscle vaso-dilatation that can be attributed to adenosine is dependent on PG synthesis. Moreover, in agreement with this, muscle vasodilatation evoked by exogenous adenosine was greatly reduced by inhibition of PG synthesis. Since there is evidence, including our own, that adenosine causes vaso-dilatation, at least in part, by releasing NO from th