Experiments were performed on anaesthetised normoxic (N) rats and chronically hypoxic (CH) rats that had been exposed to 12% O₂ for 1, 3 or 7 days. The adenosine A₁ receptor antagonist DPCPX did not affect the resting hyperventilation of 1-7 CH rats breathing 12% O₂ and increased resting heart rate (HR) in 1 CH rats only. DPCPX partially restored the decreased baseline arterial pressure (ABP) and increased femoral vascular conductance (FVC) of 1 and 3 CH rats, but had no effect in N or 7 CH rats. DPCPX also attenuated the decrease in ABP and increase in FVC evoked by acute hypoxia in N and 1-7 CH rats. The non- selective adenosine receptor antagonist 8-SPT, had no further effect on baselines or cardiovascular responses to acute hypoxia, but attenuated the hypoxia-evoked increase in respiratory frequency in 1-7 CH rats. In N, 1 and 3 CH rats, the inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine, had no effect on baselines or increases in FVC evoked by acetylcholine. We propose that (i) tonically released adenosine acting on A₁ receptors reduces HR in 1 CH rats and stimulates endothelial NOS in 1 and 3 CH rats to decrease ABP and increase FVC, the remaining NO- dependent tonic vasodilatation (Walsh & Marshall, 2006) being independent of iNOS activity. (ii) In 7 CH rats, tonic adenosine release has waned. (iii) In 1-7CH rats, adenosine released by acute hypoxia stimulates A₁ but not A₂ receptors to produce muscle vasodilatation, and stimulates carotid body A₂ receptors to increase respiration.