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Am J Physiol Gastrointest Liver Physiol 245: G64-G71, 1983;
0193-1857/83 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 245, Issue 1 64-G71, Copyright © 1983 by American Physiological Society

ARTICLES

Differentiation among inhibitory actions of omeprazole, cimetidine, and SCN- on gastric acid secretion

B. Wallmark, B. M. Jaresten, H. Larsson, B. Ryberg, A. Brandstrom and E. Fellenius

The action of the substituted benzimidazole omeprazole (H 168/68) was studied in three different in vitro preparations: the isolated guinea pig gastric mucosa, isolated intact and permeable rabbit gastric glands, and hog fundic microsomal membrane vesicles containing H+-K+-ATPase. The effects of omeprazole were compared with those of cimetidine and thiocyanate (SCN-). Under all the conditions studied, cimetidine only counteracted histamine-induced acid secretion, consonant with its H2-receptor antagonism. In contrast, omeprazole and SCN- were found not only to inhibit histamine-induced secretion but also basal acid formation and acid formation induced by dibutyryl cAMP and a high cell medium concentration of K+. Moreover, acid production induced by ATP in permeable gastric glands was antagonized by omeprazole and SCN-, whereas cimetidine was without effect. The interaction pattern of omeprazole and SCN- was differentiated by studies using the weak base antipyrine in the isolated mucosal preparation, where it was found that antipyrine could reverse the inhibition induced by SCN- but not that of omeprazole. Furthermore, omeprazole was found to inhibit the isolated H+-K+-ATPase, whereas cimetidine or SCN- was without effect. In the isolated mucosal preparation omeprazole caused an increase in K+ secretion rates in parallel with the inhibition of acid formation. This was in contrast to what was observed for cimetidine and SCN-, which exhibited no such increased K+ secretion. The results obtained from intact mucosa and isolated glands are in agreement with the ability of omeprazole to inhibit the isolated H+-K+-ATPase and thus provide evidence of a novel mechanism of action for this inhibitor.


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