Effects of Pirenzepine, Prostaglandin Analogues, and Omeprazole on Gastric Function

Abstract

Gastric acid secretion can now be inhibited by agents acting through different pathways and on different receptors. Histamine H₂-receptor antagonists dominate the field because of their apparent safety, efficacy and flexibility in clinical use. They are also at present the only drugs for long-term maintenance therapy. Selective anticholinergics acting on muscarinic receptors on parietal cells inhibit acid secretion to a lesser degree and produce some side effects of generalized parasympathetic blockade. They may proportionately inhibit pepsin more than acid and act synergistically with H₂-blockers. Prostaglandin analogues appear to act therapeutically mainly through acid inhibition. The importance of other prostaglandin effects such as cytoprotection in healing chronic duodenal ulcer is uncertain. Some of the prostaglandin analogues have produced an appreciable incidence of unwanted effects and rates of healing of duodenal ulcer have been variable. Blockade of H⁺K⁺-ATPase with omeprazole produces more and faster healing of duodenal ulcer at 2 weeks, and this appears to be a function of more profound inhibition of acid secretion. However, H₂-receptor blockers achieve similar results after somewhat longer periods of treatment. Powerful suppression of acid output seems valuable for resistant ulcers, oesophagitis, and the Zollinger-Ellison syndrome. Hypergastrinaemia does occur but should not be a problem with short-term therapy.

Key Words:

• Acid
• omeprazole
• pepsin
• pirenzepine
• prostaglandin analogues