In rings of rat iliac artery, contractions were evoked by noradrenaline (NA), the selective α1 adrenoceptor agonist phenylephrine (PE), and K+, which causes depolarisation-induced contraction. There was no evidence of α2 adrenoceptor-evoked contraction. Hypoxia, induced by reducing PO2 in the bath from 100 mmHg to 70, 55 or 40 mmHg, had similar effects on rings with (E+) and without (E-) endothelium. In E- rings, the NA concentration-response curve was biphasic, whereas that for PE was monophasic. Hypoxia reduced maximum contractions in response to NA and PE (NAmax and PEmax, respectively) without affecting the concentrations that evoked 50 % of maximum contraction (EC50). At PO2 of 70 mmHg, NAmax of the high affinity α1 receptor for NA (NAmaxh) and PEmax were reduced by ~15 %, but at PO2 of 55 and 40 mmHg, NAmaxh was severely attenuated while PEmax fell by 45 and 75 %, respectively. Similarly, the Ca2+ channel blocker nicardipine depressed NAmaxh and PEmax, but PO2 of 55 mmHg further reduced NAmax and PEmax. Hypoxia also reduced contractions evoked by NA, PE or K+ at the concentrations required to produce 80 % of the maximum contraction (EC80), receptor-mediated contractions being more affected. Ca2+-free conditions reduced the contractions evoked by NA and PE, at the EC80, to ~10 % of control. The K+ channel inhibitors glibenclamide and tetraethylammonium did not prevent hypoxia-induced depression of PE-evoked contraction. Thus, contractions evoked in iliac artery by the high affinity subtype of α1 adrenoceptor for NA, which may respond to circulating levels of NA, and by the single α1 adrenoceptor subtype for PE, are especially vulnerable to PO2 levels ≤ 55 mmHg. We propose that this reflects hypoxia-induced inhibition of Ca2+ influx through L-type and receptor-operated Ca2+ channels; K+ channel opening makes little contribution. Experimental Physiology (2002) 87.2, 171-184.