Role of gastrin and cholecystokinin receptors in regulation of peptone-stimulated gastric cid secretion in conscious rats

G. Varga, Donald R. Campbell, Louis J. Bussjaeger, Travis E. Solomon

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

With the availability of selective gastrin/CCKB (L365,260) and CCKA (L364,718) receptor antagonists the present study was designed to investigate the role of gastrin and cholecystokinin (CCK) receptors in meal-stimulated gastric acid secretion. Gastric acid output was measured by continuous intragastric titration in conscious rats. Vehicle (dimethylsulfoxide/saline, 3:1), L365,260 (3 or 9 mg/kg), or L364,718 (1 mg/kg) was given by i.v. bolus injection. Basal acid output was strongly inhibited by both doses of L365,260 while L364,718 had no effect. Intragastric peptone (4%, w/v) increased acid secretion 40-65% of the response to a maximal dose (2.5 nmol/kg per h) of gastrin-17. L365,260 completely abolished gastrin-17 stimulated acid secretion and partially inhibited peptone-induced acid secretion. Blockade of CCKA receptors by L364,718 did not affect peptone-stimulated acid output. This study demonstrates that gastrin/CCKB receptors are important in regulating basal acid secretion in the conscious rat while CCKA receptors do not appear to influence basal or peptone-stimulated gastric acid secretion. Blockade of gastrin/CCKB receptors partially inhibits intragastric meal-stimulated acid secretion indicating that the gastrin/CCKB receptor has a physiological role as mediator of food-stimulated acid secretory response in conscious rats.

Original languageEnglish
Pages (from-to)37-42
Number of pages6
JournalEuropean Journal of Pharmacology
Volume250
Issue number1
DOIs
Publication statusPublished - Nov 30 1993

Fingerprint

Cholecystokinin B Receptor
Cholecystokinin Receptors
Peptones
Stomach
Devazepide
Acids
Gastric Acid
Meals
Gastrins
Dimethyl Sulfoxide
Food
Injections

Keywords

  • CCK (cholecystokinin)
  • CCK receptor antagonist
  • Gastric acid secretion
  • Gastrin

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Role of gastrin and cholecystokinin receptors in regulation of peptone-stimulated gastric cid secretion in conscious rats. / Varga, G.; Campbell, Donald R.; Bussjaeger, Louis J.; Solomon, Travis E.

In: European Journal of Pharmacology, Vol. 250, No. 1, 30.11.1993, p. 37-42.

Research output: Contribution to journalArticle

Varga, G. ; Campbell, Donald R. ; Bussjaeger, Louis J. ; Solomon, Travis E. / Role of gastrin and cholecystokinin receptors in regulation of peptone-stimulated gastric cid secretion in conscious rats. In: European Journal of Pharmacology. 1993 ; Vol. 250, No. 1. pp. 37-42.
@article{1316e99d7a034cbea7e7e1ccfda3cd15,
title = "Role of gastrin and cholecystokinin receptors in regulation of peptone-stimulated gastric cid secretion in conscious rats",
abstract = "With the availability of selective gastrin/CCKB (L365,260) and CCKA (L364,718) receptor antagonists the present study was designed to investigate the role of gastrin and cholecystokinin (CCK) receptors in meal-stimulated gastric acid secretion. Gastric acid output was measured by continuous intragastric titration in conscious rats. Vehicle (dimethylsulfoxide/saline, 3:1), L365,260 (3 or 9 mg/kg), or L364,718 (1 mg/kg) was given by i.v. bolus injection. Basal acid output was strongly inhibited by both doses of L365,260 while L364,718 had no effect. Intragastric peptone (4{\%}, w/v) increased acid secretion 40-65{\%} of the response to a maximal dose (2.5 nmol/kg per h) of gastrin-17. L365,260 completely abolished gastrin-17 stimulated acid secretion and partially inhibited peptone-induced acid secretion. Blockade of CCKA receptors by L364,718 did not affect peptone-stimulated acid output. This study demonstrates that gastrin/CCKB receptors are important in regulating basal acid secretion in the conscious rat while CCKA receptors do not appear to influence basal or peptone-stimulated gastric acid secretion. Blockade of gastrin/CCKB receptors partially inhibits intragastric meal-stimulated acid secretion indicating that the gastrin/CCKB receptor has a physiological role as mediator of food-stimulated acid secretory response in conscious rats.",
keywords = "CCK (cholecystokinin), CCK receptor antagonist, Gastric acid secretion, Gastrin",
author = "G. Varga and Campbell, {Donald R.} and Bussjaeger, {Louis J.} and Solomon, {Travis E.}",
year = "1993",
month = "11",
day = "30",
doi = "10.1016/0014-2999(93)90618-R",
language = "English",
volume = "250",
pages = "37--42",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Role of gastrin and cholecystokinin receptors in regulation of peptone-stimulated gastric cid secretion in conscious rats

AU - Varga, G.

AU - Campbell, Donald R.

AU - Bussjaeger, Louis J.

AU - Solomon, Travis E.

PY - 1993/11/30

Y1 - 1993/11/30

N2 - With the availability of selective gastrin/CCKB (L365,260) and CCKA (L364,718) receptor antagonists the present study was designed to investigate the role of gastrin and cholecystokinin (CCK) receptors in meal-stimulated gastric acid secretion. Gastric acid output was measured by continuous intragastric titration in conscious rats. Vehicle (dimethylsulfoxide/saline, 3:1), L365,260 (3 or 9 mg/kg), or L364,718 (1 mg/kg) was given by i.v. bolus injection. Basal acid output was strongly inhibited by both doses of L365,260 while L364,718 had no effect. Intragastric peptone (4%, w/v) increased acid secretion 40-65% of the response to a maximal dose (2.5 nmol/kg per h) of gastrin-17. L365,260 completely abolished gastrin-17 stimulated acid secretion and partially inhibited peptone-induced acid secretion. Blockade of CCKA receptors by L364,718 did not affect peptone-stimulated acid output. This study demonstrates that gastrin/CCKB receptors are important in regulating basal acid secretion in the conscious rat while CCKA receptors do not appear to influence basal or peptone-stimulated gastric acid secretion. Blockade of gastrin/CCKB receptors partially inhibits intragastric meal-stimulated acid secretion indicating that the gastrin/CCKB receptor has a physiological role as mediator of food-stimulated acid secretory response in conscious rats.

AB - With the availability of selective gastrin/CCKB (L365,260) and CCKA (L364,718) receptor antagonists the present study was designed to investigate the role of gastrin and cholecystokinin (CCK) receptors in meal-stimulated gastric acid secretion. Gastric acid output was measured by continuous intragastric titration in conscious rats. Vehicle (dimethylsulfoxide/saline, 3:1), L365,260 (3 or 9 mg/kg), or L364,718 (1 mg/kg) was given by i.v. bolus injection. Basal acid output was strongly inhibited by both doses of L365,260 while L364,718 had no effect. Intragastric peptone (4%, w/v) increased acid secretion 40-65% of the response to a maximal dose (2.5 nmol/kg per h) of gastrin-17. L365,260 completely abolished gastrin-17 stimulated acid secretion and partially inhibited peptone-induced acid secretion. Blockade of CCKA receptors by L364,718 did not affect peptone-stimulated acid output. This study demonstrates that gastrin/CCKB receptors are important in regulating basal acid secretion in the conscious rat while CCKA receptors do not appear to influence basal or peptone-stimulated gastric acid secretion. Blockade of gastrin/CCKB receptors partially inhibits intragastric meal-stimulated acid secretion indicating that the gastrin/CCKB receptor has a physiological role as mediator of food-stimulated acid secretory response in conscious rats.

KW - CCK (cholecystokinin)

KW - CCK receptor antagonist

KW - Gastric acid secretion

KW - Gastrin

UR - http://www.scopus.com/inward/record.url?scp=0027508472&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027508472&partnerID=8YFLogxK

U2 - 10.1016/0014-2999(93)90618-R

DO - 10.1016/0014-2999(93)90618-R

M3 - Article

VL - 250

SP - 37

EP - 42

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1

ER -