Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion
Algazi, M.C.; Chen, H.S.; Koss, M.A.; Hogan, D.L.; Steinbach, J.; Pandol, S.J.; Isenberg, J.I.
American Journal of Physiology 256(5 Pt 1): G833-G836
1989
ISSN/ISBN: 0002-9513 PMID: 2719108 Document Number: 326962
To determine whether the recently described vasoactive intestinal peptide (VIP) antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or prostaglandin E2 (PGE2), the effects of intravenous VIP, intraluminal PGE2 and intraluminal HCl on duodenal mucosal bicarbonate secretion in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were estimated in anaesthetized rats. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by intravenous VIP and luminal acidification but not luminal PGE2. The findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP.