Swallowing induces esophageal shortening due to contraction of the longitud
inal 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 eso
phageal shortening was measured using two endoscopically affixed mucosal cl
ips. In another five cats LM contraction was measured by a strain gauge sut
ured on the serosal side at 2 cm above the LES; muscle strips from that reg
ion were obtained for in vitro studies. Swallowing induced esophageal short
ening of 48.3 +/- 8.3% and LM contraction of 4.4 +/- 0.8 g in the control p
eriod and 32.1 +/- 8% and 3.0 +/- 0.4 g after L-NAME (P < 0.05), Nitric oxi
de and SNP did not change the basal tone of esophageal LM strips but provok
ed inhibition of metacholine-induced tonic and phasic activity. Electrical
field stimulation induced frequency-dependent contractions that were reduce
d by atropine without further reduction after L-NAME, In conclusion, the re
duction of esophageal shortening after L-NAME during the in vivo experiment
s suggested an excitatory effect of NO on the feline esophagus, The in vitr
o experiments, however, showed no contractile effect of NO or SNP on LM str
ips, but an inhibitory effect on the precontracted tissue. The influence of
NO synthase blockade on in vivo esophageal LM shortening might be secondar
y to its effect on circular muscle contractility.