Integrative control of rectoanal reflex in guinea pigs through lumbar colonic nerves

The aim of the present study was to analyze the neuromodulation of rectoanal reflex activity by lumbar sympathetic nerves in guinea pigs. The mechanical activities of the rectum were recorded with a balloon connected to a pressure transducer, and those of the internal anal sphincter (IAS) were recorded with a custom-made strain gauge force transducer. Gradual and sustained rectal distension evoked the rectoanal reflex, causing cholinergic contractions of the rectum and synchronous nitrergic relaxations of the IAS. Section of the lumbar colonic nerves enhanced both rectal contractions and IAS relaxations. Section of the 13th thoracic cord abolished both rectal contractions and IAS relaxations, but section of the lumbar colonic nerves restored them. Lumbar sympathectomy and pithing sacral cords greatly diminished these rectal contractions and IAS relaxations, but the intrinsic reflex component remained. N G-nitro-l-arginine methyl ester enhanced the intrinsic reflex-mediated contraction of the rectum and abolished reflex-mediated relaxation of the IAS and converted into cholinergic contractions. The present results indicate that the extrinsic lumbar inhibitory outflow causes marked inhibition of the rectoanal reflex via the lumbar colonic nerves.

Role of neuropeptide Y in opossum internal anal sphincter

The present investigation was undertaken to examine the effects and role of neuropeptide Y (NPY) on the internal anal sphincter (IAS). The studies were performed in alpha-chloralose-anesthetized opossums. Resting pressure in the IAS (IASP) was recorded using low-compliant continuously perfused catheters. The effect of NPY administered close intra-arterially on the resting IASP was examined before and after different neurohumoral antagonists and the neurotoxin tetrodotoxin (TTX). To examine the influence of sympathetic nerves, the ventral roots of lumbar sympathetic nerves were isolated in some experiments and stimulated electrically. The influence of NPY on the IAS relaxation in response to rectoanal reflex mimicked by rectal balloon distension (RD) was also examined. NPY caused dose-dependent rise in the IASP, which was not modified by different neurohumoral antagonists and TTX. The rise in IASP by electrical stimulation of ventral lumbar nerve root (L3) was suppressed but not abolished by phentolamine. However, guanethidine (which depletes both norepinephrine and NPY) caused complete obliteration of this response. The other effect of NPY on the IAS was significant antagonism of IAS relaxation caused by RD. From these results, we conclude that NPY exerts two different actions on the IAS. First, it causes a rise in IASP by its action directly at the IAS smooth muscle. Sympathetic nerve stimulation may cause a rise in IASP by its action directly at the IAS smooth muscle partially through release of NPY. Second, it inhibits IAS relaxation produced by rectoanal reflex. These findings would suggest an important regulatory role of NPY in rectoanal physiology.