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Abstract
Female rats were treated for 1 week with ranitidine (125–1700 μmol/kg day, given subcutaneously by means of osmotic minipumps), the proton pump inhibitor ome-prazole (10–400μmol/kg day orally), or vehicle. Acid secretion, plasma gastrin levels, and oxyntic mucosal histidine decarboxylase (HDC) activity were determined. Both compounds dose-dependently inhibited maximally stimulated gastric acid secretion and caused a parallel increase in plasma gastrin levels. There was very good correlation between plasma gastrin levels and HDC activity for both compounds, although higher oxyntic mucosal HDC activity was found during ranitidine treatment. The higher HDC activity in the ranitidine-treated rats indicated the presence of a histamine H2-receptor on the ECL cells. It is concluded that, regardless of what kind of antisecretory agent is used, a dose-dependent inhibition of gastric acid secretion results in a parallel increase in plasma levels of gastrin, and as a consequence the HDC activity in the rat oxyntic mucosa is increased.