AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 256: G833-G836, 1989;
0193-1857/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Algazi, M. C.
Right arrow Articles by Isenberg, J. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Algazi, M. C.
Right arrow Articles by Isenberg, J. I.

AJP - Gastrointestinal and Liver Physiology, Vol 256, Issue 5 833-G836, Copyright © 1989 by American Physiological Society


ARTICLES

Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion

M. C. Algazi, H. S. Chen, M. A. Koss, D. L. Hogan, J. Steinbach, S. J. Pandol and J. I. Isenberg
Department of Medicine, UCSD, Medical Center.

Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. The present experiments were performed to determine whether the recently described 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 PGE2. In anesthetized rats, the effects of intravenous VIP, intraluminal PGE2, and intraluminal HCl on duodenal mucosal bicarbonate secretion both in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were measured. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. These 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.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online