Effects of H2-Receptor Antagonist on the Cellular Function of Gastric Mucosa in the Rat.
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概要
- 論文の詳細を見る
H<SUB>2</SUB>-receptor antagonists (H<SUB>2</SUB>-blockers) block the H<SUB>2</SUB>-receptors on gastric parietal cells and strongly inhibit acid secretion, resulting in an augmented gastrin secretion by gastrin (G) cells. The histamine-producing enterochromaffin-like (ECL) cells contain histidine decarboxylase (HDC), a histamine-forming enzyme, which is controlled mainly by gastrin. HDC has a short biological half-life and sensitive responses and, therefore, is a good marker for ECL cell function. To investigate the mechanisms of action of the H<SUB>2</SUB>-receptor antagonists on ECL cells, we examined the changes of gastric mucosal histamine metabolism and gastrointestinal hormones after administration of five H<SUB>2</SUB>-blockers. Cimetidine, ranitidine and nizatidine increased both the serum gastrin levels and mucosal HDC activity in a dose-manner. At high doses of famotidine and roxatidine, the gastric pH and serum gastrin levels were increased, but HDC activity was decreased. In addition, famotidine administration lowered the mucosal somatostatin levels and increased serum secretin levels. Famotidine and roxatidine may have acted directly on the ECL cells to lower the sensitivity to gastrin and suppressed HDC activity. The two H<SUB>2</SUB>-receptor antagonists, apart from their pharmacological inhibitory effect on ECL cells, may also affect cellular function of gastrin of gastric mucosa by regulating secretion of somatostatin and secretin.
- 北関東医学会の論文
著者
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Nagamachi Yukio
First Department Of Surgery
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MATSUZAKI Shigeru
Department of Biochemistry, Dokkyo University School of Medicine
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Matsuzaki Shigeru
Department Of Biochemistry Dokkyo University School Of Medicine
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Motegi Masahiko
First Department of Surgery, Gunma University School of Medicine
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