Effect of nitric oxide synthase inhibition on the acetylcholine response in the perfused hind limb of rats

The effect of nitric oxide (NO) synthase inhibition on acetylcholine-induced vasodilation in the perfused rat hind limb was investigated to find the contribution of NO to such relaxation. Although NO synthase inhibition with 150 mu g L-nitro-arginine increased vascular resistance considerably, from 7.28 +/- 0.29 to 10.83 +/- 0.44 mm Hg . min/ml (n = 7), the acetylcholine responses were not attenuated. Acetylcholine (10 mu g) induced a peak relaxation of 66 +/- 4% before, and 63 +/- 7% after L-nitro-arginine. The duration of the peak and total responses, examined in separate sets of animals (n = 12), was similar in both circumstances (61 +/- 4 s before vs. 53 +/- 5 s after, and 7.45 +/- 0.61 min before vs. 7.48 +/- 0.64 min after respectively). These results suggest that a non-NO factor is responsible for acetylcholine-stimulated relaxation in the rat hind limb vascular bed.