1986Scandinavian Journal of GastroenterologyRequires access

Effect of Acid Inhibition on Gastric Endocrine Cells

R. Arnold, H. Koop, H. Schwarting, K. Tuch, B. Willemer

Open publisher page 39 citations

Abstract

There is increasing evidence that the numbers of antral G cells and of fundic argyrophil (ECL) cells are influenced by agents that inhibit gastric acid secretion. Antral G cells increase in states of achlorhydria in man and animals provided atrophic antral gastritis is absent. In rats, treatment with substituted benzimidazoles like omeprazole and BY 308 increase G-cell densities dose-dependently. Even high doses of histamine H-2 antagonists and antacids increase antral G-cell densities. In contrast to G cells, antral D cells decrease in these instances. Fundic ECL cells increase in all experimental conditions of complete achlorhydria provided intact antral mucosa is present, i.e. there is elevated serum gastrin. Antacid treatment is not followed by an increase of fundic ECL cells, which could be explained by the less sustained increase of serum gastrin.

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What this paper is about

There is increasing evidence that the numbers of antral G cells and of fundic argyrophil (ECL) cells are influenced by agents that inhibit gastric acid secretion. Antral G cells increase in states of achlorhydria in man and animals provided atrophic antral gastritis is absent. In rats, treatment with substituted benzimidazoles like omeprazole and BY 308 increase G-cell densities dose-dependently. Even high doses of histamine H-2 antagonists and antacids increase antral G-cell densities. In contrast to G cells, antral D cells decrease in these instances. Fundic ECL cells increase in all experimental conditions of complete achlorhydria provided intact antral mucosa is present, i.e. there is elevated serum gastrin. Antacid treatment is not followed by an increase of fundic ECL cells, which could be explained by the less sustained increase of serum gastrin.

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Available abstract

There is increasing evidence that the numbers of antral G cells and of fundic argyrophil (ECL) cells are influenced by agents that inhibit gastric acid secretion. Antral G cells increase in states of achlorhydria in man and animals provided atrophic antral gastritis is absent. In rats, treatment with substituted benzimidazoles like omeprazole and BY 308 increase G-cell densities dose-dependently. Even high doses of histamine H-2 antagonists and antacids increase antral G-cell densities. In contrast to G cells, antral D cells decrease in these instances. Fundic ECL cells increase in all experimental conditions of complete achlorhydria provided intact antral mucosa is present, i.e. there is elevated serum gastrin. Antacid treatment is not followed by an increase of fundic ECL cells, which could be explained by the less sustained increase of serum gastrin.

Key concepts: Achlorhydria, G cell, Gastrin, Antrum, Enterochromaffin-like cell, Internal medicine, Enteroendocrine cell, Antacid

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