Effects of acetylcholine and nitric oxide on forearm blood flow at rest and after a single muscle contraction

We tested the hypothesis that ACh or nitric oxide (NO) might be involved in the vasodilation that accompanies a single contraction of the forearm. Eig ht adults (3 women and 5 men) completed single 1-s-duration contractions of the forearm to raise and lower a weight equivalent to similar to 20% maxim al voluntary contraction through a distance of 5 cm. In a second protocol, each subject had a cuff, placed completely about the forearm, inflated to 1 20 mmHg for a 1-s period, then released as a simulation of the mechanical e ffect of muscle contraction. Three conditions were studied, always in this order: 1) control, with intra-arterial infusion of saline; 2) after muscari nic blockade with atropine; and 3) after NO synthase inhibition with NG-mon omethyl-L-arginine (L-NMMA) plus atropine. Forearm blood flow (FBF), measur ed by combined pulsed and echo Doppler ultrasound, was reduced at rest with L-NMMA-atropine compared with the other two conditions. After the single c ontraction, there were no effects of atropine, but L-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflatio n, atropine had no effects, whereas L-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation that L-NMMA. reduced FBF in response to both cuff inflation and a brief contraction indicates that NO from the vascular endothelium might modulate the basal level of vascular tone and the mechanical component of t he hyperemia with exercise. It is unlikely that ACh and NO from the endothe lium are involved in the dilator response to a single muscle contraction.