Autonomic dysreflexia (AD) is a debilitating disorder producing episodes of extreme hypertension in patients with high level spinal cord injury (SCI). Factors leading to AD include loss of vasomotor baroreflex control to regions below injury level, changes in spinal circuitry and peripheral changes. The present study tested for peripheral changes below and above injury level 6 weeks after a T4 transection. Changes in vascular conductance were recorded in the femoral, renal, brachial and carotid arteries in response to intravenous injections of two -adrenergic agonists, phenylephrine (PE, 0.03-100µg/kg) and methoxamine (METH, 1-300µg/kg). Unlike PE, METH is not subject to neuronal re-uptake. Ganglionic blockade (chlorisondamine, 0.6mg/kg) was used to eliminate the central component of the cardiovascular response. Following ganglionic blockade SCI animals exhibited prolonged vasoconstriction in response to PE in all blood vessels measured compared to intact animals (all p<0.035). However, the PE dose-response curves obtained after ganglionic blockade revealed no significant difference in potency between the two groups (all p>0.06), indicating that the prolonged vasoconstriction was not due to supersensitivity to PE. In contrast to PE, vascular responses to METH did not vary between intact and SCI groups (all p>0.108). These results show the development of a widespread peripheral change producing prolonged vasoconstriction in response to PE, but not METH, following SCI, possibly due to reduced neuronal reuptake of PE after SCI. This is the first study to report such a change in blood vessels, not only below but also above injury level. Interventions to correct this reduced reuptake may help limit development of AD.