scholarly journals Gastric Acid Secretion Inhibition

2020 ◽  
Author(s):  
2005 ◽  
Vol 289 (1) ◽  
pp. G64-G69 ◽  
Author(s):  
Shinichi Kato ◽  
Eitaro Aihara ◽  
Katsuhide Yoshii ◽  
Koji Takeuchi

We examined the role of prostaglandin E (EP) receptor subtypes in the regulation of gastric acid secretion in the rat. Under urethane anesthesia, the stomach was superfused with saline, and the acid secretion was determined at pH 7.0 by adding 50 mM NaOH. The acid secretion was stimulated by intravenous infusion of histamine or pentagastrin. Various EP agonists were administered intravenously, whereas EP antagonists were given subcutaneously 30 min or intravenously 10 min before EP agonists. PGE2 suppressed the acid secretion stimulated by either histamine or pentagastrin in a dose-dependent manner. The acid inhibitory effect of PGE2 was mimicked by sulprostone (EP1/EP3 agonist) but not butaprost (EP2 agonist) or AE1–329 (EP4 agonist). The inhibitory effect of sulprostone, which was not affected by ONO-8711 (EP1 antagonist), was more potent against pentagastrin- (50% inhibition dose: 3.6 μg/kg) than histamine-stimulated acid secretion (50% inhibition dose: 18.0 μg/kg). Pentagastrin increased the luminal release of histamine, and this response was also inhibited by sulprostone. On the other hand, AE1–329 (EP4 agonist) stimulated the acid secretion in vagotomized animals with a significant increase in luminal histamine. This effect of AE1–329 was totally abolished by cimetidine as well as AE3–208 (EP4 antagonist). These results suggest that PGE2 has a dual effect on acid secretion: inhibition mediated by EP3 receptors and stimulation through EP4 receptors. The former effect may be brought about by suppression at both parietal and enterochromaffin-like cells, whereas the latter effect may be mediated by histamine released from enterochromaffin-like cells.


2019 ◽  
Vol 38 (Suppl. 2) ◽  
pp. 104-111 ◽  
Author(s):  
Lászlo Herszényi ◽  
Tamás Bakucz ◽  
Loránd Barabás ◽  
Zsolt Tulassay

Less than 2 centuries have elapsed since the identification of hydrochloric acid in the stomach. The clarification of the molecular mechanisms allowed the effective therapeutic suppression of gastric acid secretion. The spectacular advances in the treatment of acid-related disorders represent a synthesis of the contributions of several brilliant pharmacologists, basic scientists, and clinical physicians. Effective gastric acid suppressive therapy has dramatically improved the therapy and outcome of acid-related disorders. The introduction of proton pump inhibitors (PPIs) in clinical practice has significantly changed the medical management of upper gastrointestinal disorders. PPIs represent the “gold-standard” therapy in acid-related disorders. However, some challenges persist in the therapy of acid related diseases, including management of patients who respond inadequately to PPI therapy, more effective gastroprotection, or more powerful antisecretory treatment for the eradication of Helicobacter pylori infection. New antisecretory drugs are currently being developed and investigated to further provide a more effective and profound gastric acid secretion inhibition. The major advance has been the development of acid pump ­antagonists, the potassium channel acid blocking drugs (­P-CABs). Long-term studies comparing P-CABs with PPIs will help to define the exact place and safety profile of this class of drug in the management of acid-related disorders.


1959 ◽  
Vol 37 (2) ◽  
pp. 158-163 ◽  
Author(s):  
Horace W. Davenport ◽  
Ruth Allen

1958 ◽  
Vol 34 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Stephen J. Stempien ◽  
John D. French ◽  
Angelo Dagradi ◽  
Herbert J. Movius ◽  
Robert W. Porter

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