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Departments of Anatomy and Physiology and of Kinesiology Kansas State University, Manhattan, Kansas 66506
Few studies have examined potential
for endothelium-dependent vasodilation in skeletal muscles of different
fiber-type composition. We hypothesized that muscles composed of slow
oxidative (SO)- and/or fast oxidative glycolytic (FOG)-type fibers have
greater potential for endothelium-dependent vasodilation than muscles composed of fast glycolytic (FG)-type fibers. To test this hypothesis, the isolated perfused rat hindlimb preparation was used with a constant-flow, variable-pressure approach. Perfusion pressure was
monitored continuously, and muscle-specific flows were determined by
using radiolabeled microspheres at four time points: control, at peak
effect of acetylcholine (ACh I; 1-2 × 10
4 M),
at peak effect of ACh after infusion of an endothelial inhibitor (ACh
II), and at peak effect of sodium nitroprusside (SNP; 4-5 × 104 M). Conductance was calculated by using pressure and
flow data. In the SO-type soleus muscle, conductance increased with ACh
and SNP, but the increase in conductance with ACh was partially
abolished by the endothelial inhibitor
NG-nitro-L-arginine methyl ester
(control, 0.87 ± 0.19; ACh I, 2.07 ± 0.29; ACh II,
1.32 ± 0.15; SNP, 1.76 ± 0.19 ml · min1 · 100 g1 · mmHg1;
P < 0.05, ACh I and SNP vs. control). In the FOG-type
red gastrocnemius muscle, similar findings were obtained (control,
0.64 ± 0.11; ACh I, 1.36 ± 0.21; ACh II, 0.73 ± 0.16;
SNP, 1.30 ± 0.21 ml · min1 · 100 g1 · mmHg; P < 0.05, ACh I and SNP vs. control). In the FG-type white gastrocnemius
muscle, neither ACh nor SNP increased conductance. Similar findings
were obtained when muscles were combined into high- and low-oxidative
muscle groups. Indomethacin had no effect on responses to ACh. These
data indicate that endothelium-dependent vasodilation is exhibited by
high-oxidative, but not low-oxidative, rat skeletal muscle.
Furthermore, endothelium-dependent vasodilation in high-oxidative
muscle appears to be primarily mediated by nitric oxide.
acetylcholine; sodium nitroprusside; nitric oxide; prostaglandins
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