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1 Departments of Anatomy & Physiology and Kinesiology, Kansas State University, Manhattan, Kansas, USA
* To whom correspondence should be addressed. E-mail: mcallist{at}vet.ksu.edu.
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 comprised 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 using radiolabelled microspheres at four time points: Control, at peak effect of acetylcholine (ACH I; 1-2 X 10-4 M), at peak effect of ACH following infusion of an endothelial inhibitor (ACH II), and at peak effect of sodium nitroprusside (SNP; 4-5 X 10-4 M). Conductance was calculated 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 ml/min/100 g/mmHg; ACH I, 2.07 ± 0.29; ACH II, 1.32 ±0.15; SNP, 1.76 ± 0.19; 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 ml/min/100 g/mmHg; ACH I, 1.36 ± 0.21; ACH II, 0.73 ± 0.16; SNP, 1.30 ± 0.21; 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. Further, endothelium-dependent vasodilation in high-oxidative muscle appears to be primarily mediated by nitric oxide.
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