P. Plaisancie et al., EFFECTS OF NEUROTRANSMITTERS, GUT HORMONES, AND INFLAMMATORY MEDIATORS ON MUCUS DISCHARGE IN RAT COLON, American journal of physiology: Gastrointestinal and liver physiology, 38(5), 1998, pp. 1073-1084
The effect of potential mediators of mucus secretion was investigated
in the isolated vascularly perfused rat colon by using a sandwich enzy
me-linked immunosorbent assay for rat colonic mucin and by histochemic
al analysis. Bethanechol(100-200 mu M), bombesin (100 nM), and vasoact
ive intestinal peptide (VIP, 100 nM) provoked a dramatic mucin dischar
ge (maximal response at 900, 900, and 600% of control loops, respectiv
ely). VIP-stimulated mucin secretion was abolished by tetrodotoxin, wh
ereas atropine was without effect. In contrast, both tetrodotoxin and
atropine significantly decreased mucin release induced by bombesin. Is
oproterenol or calcitonin gene-related peptide was without effect. Ser
otonin (1-5 mu M) and peptide YY (10 nM) evoked mucin discharge, where
as glucagon-like peptide-1 did not release mucin. Finally, bromolasalo
cid (20 mu M), interleukin-1 beta (0.25 nM), sodium nitroprusside (1 m
M), and dimethyl-PGE(2) (2.5 mu M) induced mucus discharge. The result
s demonstrated a good correlation between the immunological method and
histological analysis. In conclusion, these findings suggest a role f
or the enteric nervous system, the enteroendocrine cells, and resident
immune cells in mediation of colonic mucus release.