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Gut 2002;50:786-789 doi:10.1136/gut.50.6.786
  • Helicobacter pylori

Effects of N-alpha-methyl-histamine on human H2 receptors expressed in CHO cells

  1. T Saitoh1,
  2. Y Fukushima2,
  3. H Otsuka1,
  4. M Ishikawa1,
  5. M Tamai1,
  6. H Takahashi1,
  7. H Mori1,
  8. T Asano2,
  9. M Anai2,
  10. T Ishikawa2,
  11. T Katsube3,
  12. K Ogawa3,
  13. T Kajiwara3,
  14. M Omata2,
  15. S Ohkawa1
  1. 1Department of Internal Medicine, Tokyo Women's Medical University Daini Hospital, 2-1-10 Nishiogu, Arakawa-ku, Tokyo 116-8567, Japan
  2. 2Department of Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655, Japan
  3. 3Department of Surgery, Tokyo Women's Medical University Daini Hospital, 2-1-10 Nishiogu, Arakawa-ku, Tokyo 116-8567, Japan
  1. Correspondence to:
    Dr T Saitoh, Department of Internal Medicine, Tokyo Women's Medical University Daini Hospital, 2-1-10 Nishiogu, Arakawa-ku, Tokyo 116-8567, Japan
  • Accepted 25 July 2001

Abstract

Background: Production of N-alpha-methyl-histamine (NAMH), a histamine H3 receptor (H3R) agonist, is reportedly promoted in Helicobacter pylori infected human gastric mucosa. NAMH was suggested to act directly on histamine H2 receptors (H2Rs) in animals to stimulate acid secretion and to be a H2R agonist. As H2Rs and H3Rs play different roles in gastric acid secretion, it is very important to verify that NAMH is a H2R agonist.

Aims: To determine whether NAMH is a H2R agonist, as well as a H3R agonist.

Methods: We used a Chinese hamster ovary (CHO) cell line expressing human H2Rs (CHO-H2R) and control CHO cells. Expression of human H2Rs was confirmed by tiotidine binding. cAMP production in CHO-H2R and control cells in response to histamine or NAMH was measured. cAMP production in response to 10−7 M NAMH was also measured in the presence or absence of the H2R antagonist famotidine and the H3R antagonist thioperamide.

Results: NAMH dose dependently stimulated cAMP productions in CHO-H2R cells. This production was inhibited by famotidine but not by thioperamide. Control CHO cells were unresponsive to either histamine or NAMH. In addition, the effect of NAMH, in terms of cAMP production in CHO-H2R cells, was more potent than that of histamine—that is, with a lower EC50 concentration and higher maximal cAMP production. Both NAMH and histamine, but not R-alpha-methyl-histamine, effectively inhibited [3H] tiotidine binding to CHO-H2R cells.

Conclusions: NAMH, which is produced in the gastric mucosa by H pylori, is a potent H2R agonist as well as a H3R agonist.

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