The hemodynamic tolerance of an episode of ventricular tachycardia (VT) can vary widely from no decrease in systolic blood pressure to severe hypotension. Little is known about the factors responsible for these different responses in man. Previous animal studies have suggested an important role for vasoconstriction mediated by the α-adrenergic nervous system. To determine the magnitude and time course of changes in α-adrenergic tone during symptomatic sustained monomorphic VT, VT cycle length, mean and phasic arterial pressure, forearm blood flow (by venous occlusion plethysmography) and forearm vascular resistance were measured in 15 patients. Nine of these patients were studied before and after regional intraarterial a blockade with phentolamine. After the induction of VT (350 ± 68 ms), mean forearm blood flow decreased from 3.2 ± 1.1 to 2.2 ± 0.8 ml/min/100 ml (p = 0.0002) and the forearm vascular resistance increased from 32 ± 14 to 40 ± 14 units (p = 0.01). There were no significant differences for forearm vascular resistance during the first and last 30 seconds of VT (41.3 ± 14 vs 37 ± 13 units). After the infusion of intraarterial phentolamine, there were no significant changes in the VT cycle length or mean arterial pressure, but the forearm vascular resistance increase during VT was blunted by 60 to 70%. Most patients with symptomatic VT demonstrate sympathetic vasoconstriction and these changes are maximal during the first 30 seconds of VT. This sympathoexcitatory response is due largely to stimulation of α-adrenoreceptors and may be mediated by arterial baroreflexes.