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  • Andersson, K (author)

Gastric acid secretion after depletion of enterochromaffin-like cell histamine. A study with a-fluoromethylhistidine in rats

  • Article/chapterEnglish1996

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  • 1996

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  • LIBRIS-ID:oai:lup.lub.lu.se:c0fc5776-0f2c-4336-8ad7-0030eef8d96b
  • https://lup.lub.lu.se/record/30181URI

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  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

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  • BACKGROUND: Histamine is thought to play a central role in the regulation of gastric acid secretion. In the rat oxyntic mucosa most of the histamine is synthesized and stored in enterochromaffin-like (ECL) cells, and the rest resides in mast cells. The present study examines the role of ECL-cell histamine in the control of acid secretion in the intact, conscious rat. METHODS: Rats were treated with alpha-fluoromethylhistidine (alpha-FMH) to inhibit histamine synthesis. alpha-FMH was given by continuous subcutaneous infusion (3 mg/kg/h) for up to 9 days. An additional oral dose of alpha-FMH (50 mg/kg) was given 2 h before each acid secretion test. Acid secretion was studied in pylorus-ligated rats and in chronic gastric fistula rats stimulated with histamine, gastrin-17, or insulin after 2-6 days of alpha-FMH infusion. RESULTS: Treatment with alpha-FMH lowered oxyntic mucosal histamine synthesis by 80%. From previous observations this is thought to reflect depletion of histamine from the ECL cells. The remaining 20% resides in mucosal and submucosal mast cells, which seem to be resistant to alpha-FMH. Basal acid secretion was inhibited by more than 60% after alpha-FMH treatment and by more than 80% by ranitidine. Histamine-stimulated secretion was unaffected by alpha-FMH and abolished by the histamine H2-receptor antagonist ranitidine. The acid response to gastrin-17 was almost abolished in histamine-depleted rats and abolished by ranitidine. Vagally induced acid secretion (provoked by the injection of insulin or by pylorus ligation) was unaffected by alpha-FMH treatment but abolished by ranitidine and by the muscarinic M1-receptor antagonist pirenzepine. CONCLUSION: The results suggest that gastrin stimulates acid secretion by releasing histamine from ECL cells. Vagally induced acid secretion is also dependent on a histaminergic pathway but not on ECL-cell histamine.

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  • Cabero, J L (author)
  • Mattsson, H (author)
  • Håkanson, RolfLund University,Lunds universitet,Drug Target Discovery,Forskargrupper vid Lunds universitet,Lund University Research Groups(Swepub:lu)farm-rha (author)
  • Drug Target DiscoveryForskargrupper vid Lunds universitet (creator_code:org_t)

Related titles

  • In:Scandinavian Journal of Gastroenterology31:1, s. 24-301502-7708

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By the author/editor
Andersson, K
Cabero, J L
Mattsson, H
Håkanson, Rolf
About the subject
MEDICAL AND HEALTH SCIENCES
MEDICAL AND HEAL ...
and Basic Medicine
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Scandinavian Jou ...
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Lund University

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