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. extrinsic reflex; internal anal sphincter; intrinsic reflex; pelvic nerves; rectum WE HAVE PREVIOUSLY REPORTED (22) that a rectorectal reflex is induced by prompt rectal distension in the guinea pig. This rectorectal reflex is composed of the extrinsic excitatory reflex via sacral cords (S1-3), the extrinsic inhibitory reflex via lumbar cords (L1-4), and the intrinsic cholinergic excitatory reflex via the enteric nervous system (22). The afferent and efferent limbs of the extrinsic excitatory reflex travel in the pelvic nerves, whereas the limbs of the extrinsic inhibitory reflex pass in the lumbar colonic nerves (LCNs) (22). Furthermore, we have found that the inhibitory reflex is suppressed by descending input from the pontine defecation center, leading to a disinhibition of the sacral excitatory reflex and intrinsic excitatory reflex (22)(23)(24). In view of these findings, we have proposed that the lumbar colonic inhibitory reflex contributes to the rectorectal reflex, one important component of the defecation reflex (22-25).To clarify the integrative control of the defecation reflex by the lumbar sympathetic nerves, the goal of the present study was to elucidate the rectoanal reflex [especially the rectointernal anal sphincter (recto-IAS) reflex], because the act of defecation is a consequence of successive phenomena occurring in both the colon and anorectum (9). There is considerable evidence to support the view that the descending inhibitory reflex involving inhibitory motor neurons occurs along the entire large intestine (1, 2, 6, 7). In the current study, the rectoanal reflex (especially the recto-IAS reflex) was analyzed, and the role of the lumbar sympathetic nerves in integrative control of the distension-induced rectoanal reflex was evaluated. METHODS AND MA...

The rectal distension-evoked reflex rectal (R-R) contractions and internal anal sphincter (R-IAS) relaxations in guinea pigs were generated through the extrinsic sacral excitatory nerve pathway (pelvic nerves) and the intrinsic cholinergic excitatory and nitrergic inhibitory nerve pathways. The aim of the present study was to evaluate whether a prokinetic benzamide, mosapride, enhances the R-R and R-IAS reflexes mediated via 5-HT4 receptors in the guinea pig. The mechanical activities of the R and IAS were recorded with a balloon connected to a pressure transducer and a strain gauge force transducer in the anesthetized guinea pig with intact spinal-intestinal pathways. Gradual and sustained rectal distension evoked R-R contractions and synchronous R-IAS relaxations. Mosapride (0.1-1.0 mg/kg i.v.) dose-dependently enhanced both R-R and R-IAS reflex responses. Reflex indexes for R-R and R-IAS maximally increased from 1.0 (control) to 1.92 and 1.88, respectively. A specific 5-HT4 receptor antagonist, GR 113808 (1.0 mg/kg i.v.), antagonized the enhancement of the R-R and R-IAS reflexes induced by mosapride 1.0 mg/kg i.v. The present results indicate that mosapride enhanced the R-R and R-IAS reflexes mediated through 5-HT4 receptors.

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