Role of nitric oxide during swallow-induced esophageal shortening in cats.

Swallowing induces esophageal shortening due to contraction of the longitudinal muscle (LM) layer. Experiments in the opossum have shown an excitatory effect of nitric oxide (NO) on esophageal LM strips. We evaluated the role of NO in swallow-induced esophageal shortening and assessed the effect of NO in vitro on feline LM strips. Swallow-induced esophageal shortening was studied before and after NO synthase blockade with L-NAME. In five cats esophageal shortening was measured using two endoscopically affixed mucosal clips. In another five cats LM contraction was measured by a strain gauge sutured on the serosal side at 2 cm above the LES; muscle strips from that region were obtained for in vitro studies. Swallowing induced esophageal shortening of 48.3+/-8.3% and LM contraction of 4.4+/-0.8 g in the control period and 32.1+/-8% and 3.0+/-0.4 g after L-NAME (P < 0.05). Nitric oxide and SNP did not change the basal tone of esophageal LM strips but provoked inhibition of metacholine-induced tonic and phasic activity. Electrical field stimulation induced frequency-dependent contractions that were reduced by atropine without further reduction after L-NAME. In conclusion, the reduction of esophageal shortening after L-NAME during the in vivo experiments suggested an excitatory effect of NO on the feline esophagus. The in vitro experiments, however, showed no contractile effect of NO or SNP on LM strips, but an inhibitory effect on the precontracted tissue. The influence of NO synthase blockade on in vivo esophageal LM shortening might be secondary to its effect on circular muscle contractility.