EFFECTS OF NEUROTRANSMITTERS, GUT HORMONES, AND INFLAMMATORY MEDIATORS ON MUCUS DISCHARGE IN RAT COLON

Citation
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
Citations number
35
Categorie Soggetti
Physiology
ISSN journal
01931857
Volume
38
Issue
5
Year of publication
1998
Pages
1073 - 1084
Database
ISI
SICI code
0193-1857(1998)38:5<1073:EONGHA>2.0.ZU;2-V
Abstract
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.