Abstract
1. The present study was designed to determine the mechanisms responsible for functional vasodilation of arterioles paired and unpaired with venules in the rat spinotrapezius muscle. 2. The spinotrapezius muscle (from Sprague-Dawley rats) was treated with combinations of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 100 micromol/L), the cyclo-oxygenase inhibitor indomethacin (10 micromol/L) and the epoxygenase inhibitor 6-(2-propargyloxyphenyl) hexanoic acid (PPOH; 30 micromol/L) to determine vascular responses to muscle stimulation. Both paired and unpaired arcade arterioles were chosen for microcirculatory observation. Arteriolar diameter was measured following 2 min muscle stimulation before and 30 min after subsequent application of each inhibitor. 3. In all cases, L-NAME treatment resulted in decreased basal diameter that was restored to control levels by the addition of sodium nitroprusside (0.01-0.1 micromol/L) to the superfusion solution. N(G)-Nitro-L-arginine methyl ester significantly inhibited the functional dilation in both paired (-20 +/- 3%) and unpaired (-29 +/- 3%) arterioles, whereas these inhibitory effects of L-NAME were diminished after pretreatment with indomethacin and PPOH. Indomethacin treatment attenuated the dilation in paired (-33 +/- 5%) but not unpaired (-6 +/- 4%) arterioles. Treatment with PPOH had no effect on the functional dilation in either set of arterioles. Approximately 50% of the vasodilatory responses remained in the presence of L-NAME, indomethacin and PPOH. 4. These results suggest that both nitric oxide and vasodilator prostanoid(s) are involved in mediating functional vasodilation in the rat spinotrapezius. The vasodilator prostanoid(s) released from venules is responsible for a portion of the vasodilation of the paired arteriole. The results also suggest possible interactions between the synthesis of nitric oxide and prostaglandin or epoxyeicosatrienoic acids during muscle contraction.