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Department of Exercise Science, University of Iowa, Iowa City, Iowa 52242
We sought to test the
role of nitric oxide (NO) in governing skeletal muscle (iliac) vascular
conductance during treadmill locomotion in dogs (n = 6;
3.2 and 6.4 km/h at 0% grade, and 6.4 km/h at 10% grade). As seen
previously, the increase in muscle vascular conductance accompanying
treadmill locomotion was little influenced by NO synthase inhibition
alone with N
-nitro-L-arginine
methyl ester (L-NAME, 10 mg/kg iv), but the absolute value
of conductance achieved during locomotion was reduced. Such
ambiguous results provide an unclear picture regarding the importance
of NO during locomotion. However, muscle vasodilation is normally
restrained by the sympathetic system during locomotion. Thus a
significant contribution by NO to the increase in vascular conductance
that accompanies locomotion could be masked by partial withdrawal of
the competing influence of sympathetic vasoconstrictor nerve activity
secondary to the rise in arterial pressure following systemic
L-NAME administration. To test this possibility, we
compared the rise in muscle vascular conductance before and after
L-NAME treatment while ganglionic transmission was blocked
by hexamethonium. Under these conditions, L-NAME
significantly reduced both the rise in vascular conductance (by 32%,
P < 0.001) and the absolute level of vascular
conductance (by 30%, P < 0.001) achieved during locomotion with no effect on blood flow. Thus augmented NO production normally provides a significant drive to relax vascular smooth muscle
in active skeletal muscle during locomotion. Potential deficits
stemming from the absence of NO following L-NAME treatment are masked by less intense sympathetic restraint when autonomic function is intact.
muscle blood flow; dog; iliac artery blood flow; vascular
conductance; vascular resistance; dynamic exercise; arterial pressure; hexamethonium; N-nitro-L-arginine
methyl ester
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