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 269: G138-G143, 1995;
0193-1857/95 $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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lenz, H. J.
Right arrow Articles by Silverman, T. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lenz, H. J.
Right arrow Articles by Silverman, T. A.

AJP - Gastrointestinal and Liver Physiology, Vol 269, Issue 1 138-G143, Copyright © 1995 by American Physiological Society


ARTICLES

Effects of cerebral TRH on intestinal water transport: role of vagal, muscarinic, and VIP pathways

H. J. Lenz and T. A. Silverman
Department of Medicine, University of California, San Diego, La Jolla 92093-0671, USA.

Thyrotropin-releasing hormone (TRH) is a central nervous system (CNS) transmitter that stimulates various gastrointestinal secretory and motor processes by increasing vagal outflow. In this study, the CNS effects of TRH on ileal and jejunal water transport were examined in awake rats and dogs, respectively. Cerebral but not intravenous TRH (0.1-5.0 nmol/kg) significantly (P < 0.01) reversed net water absorption from approximately 30 microliters.cm-1.h-1 in rats and 300 microliters.cm-1.h-1 in dogs toward net water secretion of 60 and 600 microliters.cm-1.h-1, respectively. Truncal vagotomy and ganglionic blockade with chlorisondamine completely abolished this stimulatory effect of cerebral TRH, whereas adrenalectomy, hypophysectomy, noradrenergic and opiate blockade, and inhibition of prostaglandin and nitric oxide synthesis did not. Atropine methylnitrate significantly (P < 0.05) attenuated the stimulatory response produced by TRH by approximately 30%. Intravenous infusion of the vasoactive intestinal peptide (VIP) receptor antagonist, [4Cl-D-Phe6, Leu17]VIP (0.05-5.0 mumol.kg-1.h-1), significantly (P < 0.01) inhibited the stimulatory response of TRH by approximately 60%. Pretreatment of the animals with both atropine and the VIP antagonist completely abolished ileal and jejunal water secretion stimulated by cerebral TRH. These results indicate that 1) TRH acts within the CNS to stimulate net ileal and jejunal water secretion in rats and dogs, respectively; 2) these actions are mediated by vagal pathways; and 3) stimulation of intestinal secretion by cerebral TRH is primarily mediated by a VIP-sensitive mechanism and, in part, by a muscarinic mechanism.


This article has been cited by other articles:


Home page
GutHome page
F H Mourad and C F Nassar
Effect of vasoactive intestinal polypeptide (VIP) antagonism on rat jejunal fluid and electrolyte secretion induced by cholera and Escherichia coli enterotoxins
Gut, September 1, 2000; 47(3): 382 - 386.
[Abstract] [Full Text] [PDF]




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