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1. The coeliac plexus can organize a gastroduodenal inhibitory reflex without action potentials. The involvement of the nitric oxide-cGMP pathway in this reflex was investigated in the rabbit on an in vitro preparation of the coeliac plexus connected to the stomach and duodenum. Intraluminal duodenal pressures were measured with water-filled balloons. Gastric distension inhibited duodenal motility, thus characterizing a gastroduodenal inhibitory reflex organized by the coeliac plexus. 2. L-Arginine, superfused at the coeliac plexus level, enhanced this reflex, whereas Nomega-nitro-L-arginine (L-NOARG) or 2-(4-carboxyphenyl)-4,4,5,5 tetramethylimidazoline-1-oxyl-3-oxide (carboxy PTIO) reduced or abolished it. Moreover, diethylamine/nitric oxide complex superfused at the coeliac plexus level inhibited duodenal motility in the absence of gastric distension. 3. The effects of nitric oxide were mediated through the activation of guanylyl cyclase, as 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) reduced or abolished the gastroduodenal inhibitory reflex, whereas zaprinast enhanced it. Moreover, 8-bromo-cGMP and cGMP, superfused at the coeliac plexus level, inhibited duodenal motility in the absence of gastric distension. 4. On the other hand, when perfused at the visceral level, L-NOARG, propranolol plus phentolamine, and guanethidine did not affect the reflex. Thus, neither nitric oxide nor noradrenaline could be the transmitters released at the muscular level to induce this reflex. 5. Our study demonstrates that the gastroduodenal inhibitory reflex, which is organized by the coeliac plexus without action potentials, is induced by the release within the plexus of nitric oxide acting on the cGMP pathway. These results provide new insights into the control of digestive motility by the prevertebral ganglia.

Propulsion in both small and large intestine is largely mediated by the peristaltic reflex; despite this, transit through the shorter colon is at least 10 times slower. Recently we demonstrated that elongating a segment of colon releases nitric oxide (NO) to inhibit peristalsis. The aims of this study were to determine if colonic elongation was physiologically significant, and whether elongation activated polarized intrinsic neural reflexes. Video imaging monitored fecal pellet evacuation from isolated guinea-pig colons full of pellets. Recordings were made from the circular muscle (CM) and longitudinal muscle (LM) in flat sheet preparations using either intracellular microelectrode or Ca2+ imaging techniques. Full colons were 158.1 ± 6.1% longer than empty colons. As each pellet was expelled, the colon shortened and pellet velocity increased exponentially (full 0.34, empty 1.01 mm s−1). In flat sheet preparations, maintained circumferential stretch generated ongoing peristaltic activity (oral excitatory and anal inhibitory junction potentials) and Ca2+ waves in LM and CM. Colonic elongation (140% of its empty slack length) applied oral to the recording site abolished these activities, whereas anal elongation significantly increased the frequency and amplitude of ongoing peristaltic activity. Oral elongation inhibited the excitation produced by anal elongation; this inhibitory effect was reversed by blocking NO synthesis. Pelvic nerve stimulation elicited polarized responses that were also suppressed by NO released during colonic elongation. In conclusion, longitudinal stretch excites specific mechosensitive ascending and descending interneurons, leading to activation of polarized reflexes. The dominance of the descending inhibitory reflex leads to slowed emptying of pellets in a naturally elongated colon.

1. Gastric relaxation, vasodilatation and vasoactive intestinal peptide (VIP) output from the stomach in response to stimulation of the central end of the cut vagus nerve were studied in anaesthetized dogs. 2. Central vagal stimulation (10 Hz, 40 V, 0.5 ms) normally produced a non-adrenergic, non-cholinergic (NANC) gastric relaxation via a vago-vagal reflex. It also caused an increase followed by a decrease in gastric blood flow. 3. The increase in blood flow was attributable to a NANC gastric vasodilatation via a vago-vagal reflex and the subsequent reduction in blood flow was decreased by splanchinicotomy. All these gastric and vascular responses were abolished by hexamethonium. 4. The gastric relaxation and vasodilatation induced by the vago-vagal reflex had similar stimulation frequency-response and pulse duration-response relations. 5. Central vagal stimulation caused an increase in gastric venous VIP output which was abolished by vagotomy or hexamethonium but unaffected by splanchnicotomy. 6. VIP injected into the gastric artery mimicked the gastric relaxant and vasodilator responses to the vago-vagal reflex. 7. We conclude that the intramural NANC inhibitory nerves activated by the vago-vagal reflex release VIP which causes both gastric relaxation and vasodilatation.

1. In the urethane anaesthetized ferret gastric inflation with 50 ml. 0.9% NaCl at a rate of 10 ml./min evoked large gastric contractions. The threshold of intragastric pressure required to elicit the reflex was 3.1 +/- 0.5 cmH2O. 2. The response was enhanced by splanchnic nerve section and markedly reduced by bilateral cervical vagotomy, indicating that both afferent and efferent limbs of the reflex were in the vagus nerves. 3. By using a transected stomach it was shown that distension of the corpus evoked contractions of the antrum that were abolished by vagotomy. 4. The reflex activation of antral motility by vagal afferents with receptive fields in the corpus may play a physiological role in gastric emptying.