Duodenal wall motility, mucosal net fluid and alkaline secretion in response to luminal acid: role of the vagal nerves and cholinergic transmission

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Abstract
Experiments were performed on chloralose anaesthetized cats. Biliary and pancreatic secretions were diverted by separate cannulation of each duct. A 2-cm segment of the proximal duodenum was isolated between two luminally situated balloons and perfused with isotonic saline containing 14C-PEG 4000 as a non-absorbable marker. The perfusate was analysed with regard to alkalinity (back titration) and concentration of marker (liquid scintillation). Net alkalinization and net fluid transport were calculated with conventional equations. Motor activity in the duodenal wall was recorded as changes in volume of the proximal balloon. Exposing the duodenal segment of 30 mM HCl induced duodenal contractions, net fluid secretion and an increased alkaline secretion, responses which were insensitive to acute truncal vagotomy. The acid-induced increase in contraction frequency was inhibited by hexamethonium, but not by atropine. Alkaline secretion in response to luminal acid was blocked by hexamethonium and inhibited by atropine, whereas the net fluid secretion was insensitive to these compounds. It is concluded that luminal exposure to hydrochloric acid changes the duodenal functional state by mechanisms which are independent of the extrinsic neural supply. Duodenal contractions during luminal acid exposure, and the alkalinization after such acid exposure, are mediated via local neural pathways, involving a nicotinic cholinergic step and, to some degree, muscarinic transmission. The mucosal volume secretion, however, appears to be mediated by non-conventional mechanisms.