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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Oct 2007|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)