Alteration of H2 receptor sensitivity in duodenal ulcer patients after maintenance treatment with an H2 receptor antagonist

D. B. Jones, Colin Howden, D. W. Burget, C. Silletti, R. H. Hunt

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

The effects of a specific H2 receptor agonist impromidine, on gastric acid secretion were measured in six patients with duodenal ulcer in clinical remission before and after three months treatment with ranitidine 150 mg nocte. After treatment basal acid output increased from 1.2 to 2.8 mmol/h and after maximal impromidine stimulation from 36.9 (4.7) to 44.2 (6.2) mmol/h (p < 0.02). Intravenous ranitidine 50 mg was given at the end of the impromidine infusion on each study day; the antisecretory effect of intravenous ranitidine was accentuated after the treatment with ranitidine from a trough acid output of 8.5 (1.2) mmol/h before, to 3.8 (1.5) mmol/h (p < 0.05) after, treatment. The increased response to the H2 agonist impromidine and the H2 antagonist ranitidine after treatment with ranitidine suggests an enhanced sensitivity of the H2 receptor. This might be explained on the basis of an increase in the number of H2 receptors ('up-regulation').

Original languageEnglish (US)
Pages (from-to)890-893
Number of pages4
JournalGut
Volume29
Issue number7
DOIs
StatePublished - Jan 1 1988

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Histamine H2 Receptors
Ranitidine
Impromidine
Duodenal Ulcer
Histamine Agonists
Therapeutics
Acids
Gastric Acid
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Alteration of H2 receptor sensitivity in duodenal ulcer patients after maintenance treatment with an H2 receptor antagonist. / Jones, D. B.; Howden, Colin; Burget, D. W.; Silletti, C.; Hunt, R. H.

In: Gut, Vol. 29, No. 7, 01.01.1988, p. 890-893.

Research output: Contribution to journalArticle

Jones, D. B. ; Howden, Colin ; Burget, D. W. ; Silletti, C. ; Hunt, R. H. / Alteration of H2 receptor sensitivity in duodenal ulcer patients after maintenance treatment with an H2 receptor antagonist. In: Gut. 1988 ; Vol. 29, No. 7. pp. 890-893.
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