THE ROLE OF NON-ADRENERGIC NON-CHOLINERGIC SYSTEM IN THE PERISTALTIC REFLEX OF GUINE A PIG ILEUM

The effect of some endogenous components -endogenous opiates, cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP) and somatostatin-as inhibitory or excitatory transmitters in the local nervous pathways involved in peristaltic responses was examined. The peristaltic reflex was studied using a modification of the Trendelenberg preparation. In each preparation, the luminal distension pressure was increased in sudden steps of I cm H20 at intervals of 10, until peristalsis was initiated. Morphine inhibited the rhythmic peristaltic activity. The inhibitory effect of morphine was characterized by a decreased activity of both the longitudinal and circular muscle layers. Addition of naloxone to the organ bath reversed this inhibitory effect of morphine. Using distension pressures which evoke only tetrodotoxin-sensitive peristaltic contractions, the mechanism rapidly "fatigues". This fatigue can be reversed by naloxone. Higher distending pressure, which can evoke tetrodotoxin-resistant activity, produced persistent peristalsis with intermittent activity seize. Addition of naloxone reversed the b lockade leading to a continuous uninterrupted peristalsis. Proglumide ordbcGMP (selective inhibitor of the effects of CCK) increased the threshold pressure necessary to cause the peristaltic reflex and blocked all responses to threshold distension .. Cholecystokinin or caerulein decreased the threshold of distension pressure required to evoke the peristaltic reflex. Furthermore, it increased the height and duration of the responses. The excitatory effect of CCK or caerulein was blocked by proglumide or dbcGMP. VIP increased the threshold of distension required to cause the peristaltic reflex and blocked the responses to threshold distension of longitudinal but not circular muscle layers. Somatostatin has been proved to exert an unusual effect on peristalsis. At high concentration it decreased the duration of the responses but had no effect on the height of rhythmic activity. It is concluded that the activation of intramural neurones by distension causes the release of inhibitory and excitatory transmitters, such as endogenous opiates which interrupts peristaltic activity and CCK which enhance the peristaltic reflex at a synapse with cholinergic neurones since CCK releases acetylcholine from intrinsic nerves. VIP and somatostatin are involved in the peristaltic reflex but the mechanism of their actions are not studied in this work.