Advances in drug therapy for peptic ulcer disease.
Recently, three new drug types have emerged to treat peptic ulceration. We compared the mechanism of action of omeprazole and somatostatin-14, both inhibitors of gastric acid, with that of tetraprenylacetone, a drug thought to be cytoprotective in the upper gut. Omeprazole and somatostatin-14 caused potent inhibition of meal-stimulated acid secretion in the dog (92% +/- 6% and 97% +/- 1%, respectively). On the other hand, tetraprenylacetone had no significant inhibitory effect on acid secretion (4% +/- 17%). In separate studies, tetraprenylacetone was shown to be a stimulant of gastric bicarbonate secretion in the rabbit, increasing bicarbonate secretion from a basal level of 0 to 86 +/- 28 pmol/2 h. Tetraprenylactone was also found to be a strong stimulant of canine pancreatic bicarbonate secretion. The ability of tetraprenylacetone to stimulate endogenous bicarbonate secretion may explain its ability to heal ulcers both experimentally and clinically.
D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001639:Bicarbonates / Q000378:metabolism*; D004224:Diterpenes / Q000494:pharmacology; D004285:Dogs; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects; D009853:Omeprazole / Q000494:pharmacology; D010179:Pancreas / Q000187:drug effects; D010437:Peptic Ulcer / Q000188:drug therapy* / Q000378:metabolism; D011817:Rabbits; D013004:Somatostatin / Q000494:pharmacology; D013223:Statistics as Topic
D000897:Anti-Ulcer Agents; D001639:Bicarbonates; D004224:Diterpenes; D013004:Somatostatin; D009853:Omeprazole; C031049:geranylgeranylacetone