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1986•Scandinavian Journal of GastroenterologyRequires access

Mechanism of Inhibition of H+K+ATPase by Omeprazole

B. Wallmark, Arne Brändström, Håkan Larsson

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Abstract

Omeprazole has been found to be a potent inhibitor of gastric acid secretion in several species, including man (1–3). The in vitro inhibitory effect of omeprazole on gastric acid secretory functions has been reported in isolated mucosal, glandular and enriched parietal cell preparations. Omeprazole counteracted not only basal acid formation but also acid production induced by various secretagogues (4–9). Furthermore, when assayed in permeable gastric glands, omeprazole inhibited the secretory response induced by ATP and K+. This indicates that the site of action of omeprazole is distal to that of second messenger production, and probably close to the proton pump site.

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What this paper is about

Omeprazole has been found to be a potent inhibitor of gastric acid secretion in several species, including man (1–3). The in vitro inhibitory effect of omeprazole on gastric acid secretory functions has been reported in isolated mucosal, glandular and enriched parietal cell preparations. Omeprazole counteracted not only basal acid formation but also acid production induced by various secretagogues (4–9). Furthermore, when assayed in permeable gastric glands, omeprazole inhibited the secretory response induced by ATP and K+. This indicates that the site of action of omeprazole is distal to that of second messenger production, and probably close to the proton pump site.

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OpenAlex reports 29 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

Omeprazole has been found to be a potent inhibitor of gastric acid secretion in several species, including man (1–3). The in vitro inhibitory effect of omeprazole on gastric acid secretory functions has been reported in isolated mucosal, glandular and enriched parietal cell preparations. Omeprazole counteracted not only basal acid formation but also acid production induced by various secretagogues (4–9). Furthermore, when assayed in permeable gastric glands, omeprazole inhibited the secretory response induced by ATP and K+. This indicates that the site of action of omeprazole is distal to that of second messenger production, and probably close to the proton pump site.

Key concepts: Omeprazole, Parietal cell, Gastric acid, Secretion, Proton-pump inhibitor, ATPase, Chemistry, H(+)-K(+)-Exchanging ATPase

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