© 2002 by Gut
COMMENTARY
Heliocobacter pylori
Easy as 1, 2, 3? Histamine receptors and gastric acid
1 School of Medicine, Health Policy and Practice, University of East Anglia, Norwich NR4 7TJ, UK;i.beales@uea.ac.uk
N-alpha-methyl-histamine, which is produced in the gastric mucosa by Helicobacter pylori, is a potent H2 receptor agonist as well as a H3 receptor agonist
Keywords: Chinese hamster ovary cells; histamine H2 receptors; histamine H3 receptors; N-alpha-methyl-histamine; UGT1A7; xenobiotic metabolism; environmental carcinogens; colorectal cancer; UGT1A gene locus; allelic association
It is over 80 years since the stimulatory effect of histamine on gastric acid was reported.1 The observation that the conventional antihistamines (subsequently shown to be H1 antagonists) failed to block the acid stimulatory action2 ultimately led to the discovery and availability of H2 antagonists.3 These were not only effective drugs but tools to dissect acid secretory physiology, and develop our continually evolving paradigm of histamine as the major paracrine stimulant of gastric acid.4
In the gastric mucosa, histamine is found within enterochromaffin-like (ECL) cells and mast cells, the relative proportion of the two cell types being species and site dependent. Histamine is formed by the decarboxylation of histamine by histidine decarboxylase (HDC). After release histamine is enzymatically deactivated by two pathways. The majority is methylated onto one of the nitrogen atoms in the imidazole ring by imidazole-N-methyltransferase, and a smaller proportion is degraded by oxidative
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Gut 2002 50: 786-789.
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