In patients with high thoracic spinal lesions that remove most of the central drive to splanchnic preganglionic neurones, visceral or nociceptive stimuli below the lesion can provoke large increases in blood pressure (autonomic dysreflexia). Here the effects of T4 spinal transection on isometric contractions of mesenteric arteries isolated from spinalized rats were examined. Nerve-evoked contractions involved synergistic roles for norepinephrine and ATP. Seven weeks after spinal transection, responses to perivascular stimulation at 1-5 Hz were enhanced 5-fold while the ₁-adrenoceptor antagonist, prazosin (10 nM), produced a 2-fold larger reduction in contraction to 20 pulses at 10 Hz than in unoperated controls. In contrast, the reduction in nerve-evoked contractions by the P2-purinoceptor antagonist, suramin (0.1 mM), and the responses to the P2-purinoceptor agonist, ,-methylene ATP, or to high [K⁺], did not greatly differ between groups, indicating that arteries from spinalized rats were not generally hyperreactive. Sensitivity to the ₁-adrenoceptor agonist, phenylephrine, was enhanced in arteries from spinalized rats and the difference from controls was abolished by the norepinephrine uptake blocker, desmethylimpramine. Further, the groups had similar sensitivity to the ₁-adrenoceptor agonist, methoxamine, which is not a substrate for the neuronal norepinephrine transporter. Thus the increased neurally evoked response after spinal transection appeared to be due to a reduction in neuronal uptake of released norepinephrine, a mechanism that did not explain the enhanced response of tail arteries after spinal transection that we previously reported. The findings provide further support for potentiated neurovascular responses contributing to the genesis of autonomic dysreflexia.