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- Title
Nα-methyl histamine and histamine stimulate gastrin release from rabbit G-cells via histamine H<sub>2</sub>-receptors.
- Authors
Bliss; Healey; Arebi; Calam
- Abstract
Background: Gastrin release by Helicobacter pylori may be an important step in the pathway leading to duodenal ulceration. A histamine H3-receptor agonist was found to release gastrin from antral mucosal fragments; this was interpreted as being due to suppression of somatostatin release. H. pylori is reported to produce Nα-methyl histamine (NαMH), which is an agonist of H3 as well as other histamine receptors. H. pylori infection also recruits mast cells, which release histamine. Aim: To determine the direct effects of histamine receptor agonists on isolated gastrin cells. Methods: Rabbit G-cells were prepared by countercurrent elutriation and cultured on 24-well plates. Results: NαMH (10–6–10–4 M) caused a dose-dependent increase in gastrin release from a basal level of 2.3 ± 0.2% total cell content (TCC; mean ± S.E.M.) to a maximum of 5.1 ± 0.7%, an increase of 117% (P < 0.005) above basal. This was abolished by the H2-antagonist ranitidine (10–5 M), but not by immunoblockade with anti-somatostatin antibody, the H1-antagonist chlorpheniramine (10–5 M) or the H3-antagonist thioperamide (10–4 M). The histamine H2-receptor agonist dimaprit (10–6–10–4 M) increased gastrin release from 2.4 ± 0.2% to 3.6 ± 0.2% TCC (P < 0.001). Gastrin release was also stimulated by histamine (10–7–10–4 M) from a basal value of 3.0 ± 0.3% to 5.4 ± 0.5% TCC (P < 0.001). This also was inhibited by ranitidine (10–5 M) (P < 0.01). Conclusion: NαMH and histamine release gastrin from G-cells via H2-receptors; this might contribute to H. pylori-associated hypergastrinaemia.
- Subjects
HISTAMINE; GASTRIN; GASTRIC mucosa; HELICOBACTER pylori infections
- Publication
Alimentary Pharmacology & Therapeutics, 1999, Vol 13, Issue 12, p1669
- ISSN
0269-2813
- Publication type
Article
- DOI
10.1046/j.1365-2036.1999.00649.x