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Gastroenterology Research Unit, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan 48109-0682
We recently
demonstrated that luminal factors such as osmolality, disaccharides,
and mechanical stimulation evoke pancreatic secretion by activating
5-hydroxytryptamine subtype 3 (serotonin-3, 5-HT3)
receptors on mucosal vagal afferent fibers in the intestine. We
hypothesized that 5-HT released by luminal stimuli acts as a paracrine
substance, activating the mucosal vagal afferent fibers to stimulate
pancreatic secretion. In the in vivo rat model, luminal perfusion of
maltose or hypertonic NaCl increased 5-HT level threefold in intestinal
effluent perfusates. Similar levels were observed after intraluminal
10
5 M 5-HT perfusion. These treatments did not affect
5-HT blood levels. In a separate study, intraduodenal, but not
intraileal, 5-HT application induced a dose-dependent increase in
pancreatic protein secretion, which was not blocked by the CCK-A
antagonist CR-1409. Acute vagotomy, methscopolamine, or perivagal or
intestinal mucosal application of capsaicin abolished 5-HT-induced
pancreatic secretion. In conscious rats, luminal 105 M
5-HT administration produced a 90% increase in pancreatic protein output, which was markedly inhibited by the 5-HT3
antagonist ondansetron. In conclusion, luminal stimuli induce 5-HT
release, which in turn activates 5-HT3 receptors on mucosal
vagal afferent terminals. In this manner, 5-HT acts as a paracrine
substance to stimulate pancreatic secretion via a vagal cholinergic pathway.
vagal afferent; enterochromaffin cell; intestinal luminal nutrient; rat
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