Neuronal influence on intestinal transport.

Reflex activation of the enteric nervous system (ENS) from the intestinal lumen and also from the serosa induces intestinal secretion. Thus mechanical distention, cholera toxin, heat-stable enterotoxin from E. coli, bile acids, mucosal inflammation and chemical peritonitis all induce an intestinal secretion that is inhibited by 60-100% by nerve-blocking agents. As a result of a large number of in vitro and in vivo studies, a picture of the organization of the secretory enteric nervous reflexes is now emerging. In secretory states with preserved intact intestinal epithelium, it is proposed that the reflex activation occurs via stimulation of receptor cells, i.e. epithelial endocrine cells such as EC and N-cells, which release peptides/amines into the interstitial space and thereby activate nerves close to the epithelium. The afferent neurones appear to transfer the reflex to the myenteric plexus, probably by using tachykinins as transmitters. This is in agreement with a superior and co-ordinating role for the myenteric plexus in the control of intestinal function by the ENS. Interneurones in turn mediate the transmission of the nerve signal to the submucosal plexus and the efferent neurones via cholinergic, nicotinic postganglionic receptors. The transmitters at the effector cells are acetylcholine and probably VIP.