Gastric antiulcer activity of calcium channel blockers in rats

Abstract

This study has been undertaken to elucidate the possible mechanism of action of calcium channel blockers (CCBs) such as verapamil, nifedipine and diltiazem against experimentally induced gastric ulcers. The parameters studied include volume of gastric secretion, free and total acidity, pepsin activity, ulcer index, gastric wall mucus content, dissolved mucosubstances of gastric juice such as total carbohydrates (total hexose, hexosamine, fucose and sialic acid) and protein content of gastric juice using aspirin plus pylorus ligation (PL) model. CCBs significantly increased total carbohydrates of gastric juice. The protein content of gastric juice was significantly decreased. Thus a rise was observed in TC:PR ratio. Insoluble gastric wall mucus content was found to be increased in presence of CCBs. These results suggest that CCBs may act through prevention of gastric mucosal damage thereby strengthening the mucosal barrier