Introduction: The esophagus is subject to frequent reflux of gastric contents as a normal phenomenon during episodes of transient lower esophageal sphincter relaxation (tLESR), responsible too, for pathologic reflux. However, pathologic reflux is mostly associated with reflux of acid contents. Distending the stomach provokes an increase in frequency of tLESR. Objective: To investigate the effect of distending the rectum on the tLESR and possible involved pathways. Methods: Forty four (Protocol: 096/07) street dogs were selected and divided into respective protocols: Rectal distention (RD), Gastric distention (GD), RD+GD, Atropine+RD, Hexamethonium+RD, Baclofen+RD, Bilateral Pudendal nerve section+RD and Spinal cord transection+RD. We determined and compared the tLESR of each group and subjected data to statistical analysis. Values of p<0.05 were regarded as statistically significant. Results: RD provoked a significant increase in the tLESR just as GD, with RD+GD provoking the highest value of tLESR. This increase in tLESR due to RD was prevented in A+RD, B+RD, Bilateral Pudendal nerve section+RD and Spinal cord transection+RD but not Hexamethonium+RD protocols. Conclusion: RD is a significant inducer of an increase in tLESR with participation of muscharinic and GABAβ, sensitive and spinal cord neurons, but not nicotinic receptors.
