Metabolic forearm vasodilation is enhanced following Bier block with phentolamine

The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O₂ fraction = 0.1) before and after regional sympathetic blockade with the α-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with α-receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 ± 0.05 vs. 1.03 ± 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 ± 0.14 vs. 0.53 ± 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 ± 75 vs. 826 ± 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 ± 66 vs. 661 ± 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 ± 0.06 vs. 1.16 ± 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 ± 0.16 vs. 0.87 ± 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O₂ saturation = 77 ± 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.