Does autonomic blockade reveal a potent contribution of nitric oxide to locomotion-induced vasodilation?

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