Document Detail


Role of gastrin, histamine, and acetylcholine in the gastric phase of acid secretion in anesthetized rats.
MedLine Citation:
PMID:  1348909     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To determine the relative contributions of gastrin, histamine, and cholinergic stimulation to the gastric phase of acid secretion, peptone-stimulated acid output was measured in urethan-anesthetized pylorus-ligated rats after intravenous administration of gastrin monoclonal antibody, cimetidine, and atropine. Intragastric peptone stimulated acid secretion four-fold over basal, which was associated with a significant increase in plasma gastrin levels. Gastrin immunoneutralization and simultaneous H2- and muscarinic-receptor blockade demonstrated that approximately 40% of peptone-stimulated acid output as attributed to endogenous gastrin through a histamine-dependent pathway, whereas 20% of acid output was accounted for by a cholinergic component. Another 10% of titratable acid was omeprazole-insensitive and presumably due to intragastric digestion of peptone. Therefore, approximately 30% residual acid output in response to peptone could not be accounted for by known acid stimulatory mechanisms. In rats given somatostatin monoclonal antibody to block the tonic inhibitory effect of endogenous somatostatin, residual acid output was a similar fraction of meal-stimulated acid output. In contrast, gastric distension induced by intragastric instillation of saline stimulated acid secretion to 1.5-fold over basal. Although 60% of distension-induced acid secretion could be inhibited by either H2 blockade or gastrin immunoneutralization, acid output returned to basal levels after simultaneous muscarinic blockade. These results indicate that gastrin, through a histaminergic pathway, is the principal mediator of meal-stimulated acid secretion in anesthetized rats. Approximately 30% of acid output was due to other unidentified mechanisms, such as chemical secretagogues, a direct effect of amino acids, or novel peptides.
Authors:
K C Lloyd; H E Raybould; Y Taché; J H Walsh
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  262     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1992 Apr 
Date Detail:
Created Date:  1992-05-21     Completed Date:  1992-05-21     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  G747-55     Citation Subset:  IM    
Affiliation:
Research Service, Department of Veterans Affairs, Los Angeles, California.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / physiology*
Animals
Antibodies, Monoclonal
Bethanechol
Bethanechol Compounds / pharmacology
Gastric Acid / secretion*
Gastrins / antagonists & inhibitors,  blood,  pharmacology,  physiology*
Histamine / pharmacology,  physiology*
Male
Omeprazole / pharmacology
Rats
Rats, Inbred Strains
Somatostatin / immunology
Grant Support
ID/Acronym/Agency:
DDK-41301/DK/NIDDK NIH HHS; DK-17294/DK/NIDDK NIH HHS; MH-00663/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Bethanechol Compounds; 0/Gastrins; 51-45-6/Histamine; 51-84-3/Acetylcholine; 51110-01-1/Somatostatin; 60748-06-3/gastrin 17; 674-38-4/Bethanechol; 73590-58-6/Omeprazole

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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