Patients with severe spinal cord lesions that damage descending autonomic pathways generally have low resting arterial pressure but bladder or colon distension or unheeded injuries may elicit a life-threatening hypertensive episode. Such episodes (known as autonomic dysreflexia) are thought to result from the loss of descending baroreflex inhibition and/or plasticity within the spinal cord. However, it is not clear whether changes in the periphery contribute to the exaggerated reflex vasoconstriction. The effects of spinal transection at T7 - 8 on nerve- and agonist-evoked contractions of the rat tail artery were investigated in vitro. Isometric contractions of arterial segments were recorded and responses of arteries from spinalized animals (spinalized arteries) and age-matched and sham-operated controls were compared. Two and eight weeks after transection, nerve stimulation at 0.1 - 10 Hz produced contractions of greater force and duration in spinalized arteries. At both stages, the a-adrenoceptor antagonists, prazosin (10 nM) and idazoxan (0.1 µM), produced less blockade of nerve-evoked contraction in spinalized arteries. Two weeks after transection, spinalized arteries were supersensitive to the a1-adrenoceptor agonist, phenylephrine, and the a2-adrenoceptor agonist, clonidine, but, eight weeks after transection, spinalized arteries were supersensitive only to clonidine. Contractions of spinalized arteries elicited by 60 mM K+ were larger and decayed more slowly at both stages. These findings demonstrate that spinal transection markedly increases nerve-evoked contractions and this can, in part, be accounted for by increased reactivity of the vascular smooth muscle to vasoconstrictor agents. This hyperreactivity may contribute to the genesis of autonomic dysreflexia in patients.