PMID- 9813278
OWN - NLM
STAT- MEDLINE
DCOM- 19990129
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 810
IP  - 1-2
DP  - 1998 Nov 9
TI  - Pretreatment with SR48692 has different effects on central neurotensin-induced 
      gastric mucosal defense and inhibition of gastric acid secretion in rats.
PG  - 123-9
AB  - Neurotensin is a tridecapeptide present in the brain and gastrointestinal tract. 
      Administration of neurotensin into the brain results in responses in the 
      gastrointestinal tract, suggesting a role for neurotensin in the 
      interrelationships that comprise the brain-gut axis. Intracerebroventricular 
      (i.c.v.) administration of neurotensin protects the gastric mucosa against injury 
      caused by cold water restraint (CWR) and also inhibits gastrin-stimulated gastric 
      acid secretion. The hypothesis tested was that these two actions of neurotensin 
      are mediated via its high-affinity receptor. Rats were given neurotensin (60 
      microgram, i.c.v.) prior to CWR or pylorus ligation after pretreatment with 
      SR48692, a nonpeptide antagonist of the high-affinity neurotensin receptor (0.25 
      or 2.5 microgram, i.c.v., or 10, 100, or 500 microgram kg-1, i.p.). Neurotensin 
      reduced cold water restraint (CWR)-induced gastric mucosal injury and inhibited 
      gastrin-stimulated acid secretion. Pretreatment with SR48692 (2.5 microgram, 
      i.c.v., or 100 microgram kg-1, i.p.) prior to CWR blocked neurotensin's 
      protection of the gastric mucosa against injury. In contrast, pretreatment with 
      2.5 microgram SR48692, i.c.v., did not block neurotensin-induced inhibition of 
      acid secretion, whereas 500 microgram kg-1, i.p., partially blocked the 
      inhibition. SR48692 (2.5 microgram, i.c.v.) inhibited acid secretion, suggesting 
      that SR48692 has agonist activity in this system. These results suggest that 
      central neurotensin protects the gastric mucosa against CWR-induced injury via 
      its high-affinity receptor. The receptor that mediates central 
      neurotensin-induced inhibition of gastric acid secretion does not appear to be 
      the high-affinity receptor since the neurotensin receptor antagonist SR48692, 
      when given i.c.v., had agonist activity, inhibiting stimulated acid secretion. 
      High-affinity neurotensin receptors in the periphery appear to play a role in 
      inhibition of stimulated gastric acid secretion.
CI  - Copyright 1998 Elsevier Science B.V.
FAU - Karinch, A M
AU  - Karinch AM
AD  - Division of General Surgery, Department of Surgery, The Pennsylvania State 
      University College of Medicine, P.O. Box 850, Hershey, PA 17033, USA.
FAU - Schmidt, G L
AU  - Schmidt GL
FAU - Kauffman, G L Jr
AU  - Kauffman GL Jr
LA  - eng
GR  - DK-38198-05/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Anti-Ulcer Agents)
RN  - 0 (Pyrazoles)
RN  - 0 (Quinolines)
RN  - 0 (Receptors, Neurotensin)
RN  - 146362-70-1 (SR 48692)
RN  - 39379-15-2 (Neurotensin)
RN  - EF0NX91490 (Pentagastrin)
SB  - IM
MH  - Animals
MH  - Anti-Ulcer Agents/administration & dosage/*pharmacology
MH  - Cold Temperature
MH  - Gastric Acid/*metabolism
MH  - Gastric Mucosa/*drug effects/metabolism
MH  - Injections, Intraperitoneal
MH  - Injections, Intraventricular
MH  - Male
MH  - Neurotensin/administration & dosage/*pharmacology
MH  - Pentagastrin/pharmacology
MH  - Pylorus/physiology
MH  - Pyrazoles/*pharmacology
MH  - Quinolines/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Neurotensin/*antagonists & inhibitors
MH  - Restraint, Physical
MH  - Stress, Psychological/physiopathology
EDAT- 1998/11/14 03:01
MHDA- 2001/03/28 10:01
CRDT- 1998/11/14 03:01
PHST- 1998/11/14 03:01 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1998/11/14 03:01 [entrez]
AID - S0006-8993(98)00896-8 [pii]
AID - 10.1016/s0006-8993(98)00896-8 [doi]
PST - ppublish
SO  - Brain Res. 1998 Nov 9;810(1-2):123-9. doi: 10.1016/s0006-8993(98)00896-8.