CHOLINERGIC REGULATION OF HUMAN PROXIMAL DUODENAL MUCOSAL BICARBONATE SECRETION

Cephalic-vagal stimulation affects a number of upper gastrointestinal secretory and motility events. The purpose of this study was to examine the role of vagal-cholinergic regulation on human proximal duodenal mucosal HCO3- secretion. The duodenal bulb was isolated between balloons and perfused with 154 mM NaCl, and HCO3- secretion was measured. Although cholinergic stimulation with bethanechol (50-mu-g.kg-1.h-1 iv) produced systemic effects, resting HCO3- secretion was unchanged. Cephalic-vagal stimulation, induced by sham feeding, significantly increased duodenal HCO3- secretion from a basal of 177 +/- 17 to 240 +/- 19-mu-mol.cm-1.h-1 (P < 0.02). The response to sham feeding was approximately 50% of the peak response to acid-stimulated HCO3- output. Atropine (22-mu-g/kg iv) inhibited basal HCO3- secretion significantly (79 +/- 5%). However, the net incremental increases in duodenal mucosal HCO3- secretion in response to luminal acidification and vagal stimulation were unaltered by atropine pretreatment. Additionally, indomethacin (100 mg po) failed to modify the response to vagal-stimulated HCO3- secretion. These findings indicate that basal human proximal duodenal mucosal HCO3- secretion is maintained largely by resting cholinergic innervation and is stimulated by cephalic-vagal stimulation. Furthermore, since the incremental HCO3- responses to cephalic-vagal stimulation and luminal acidification were unaltered by atropine pretreatment, each is likely mediated by noncholinergic mechanisms.