Release of endogenous prostaglandins by mild hyperosmotic saline inhibits tetragastrin-stimulated gastric acid secretion in rats |
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| Authors: | Yutaka Suzuki Yoshiteru Harada Akinori Ueno Makoto Katori Haruya Okabe |
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| Affiliation: | 1. College of Food Science, Southwest University, 2 Tiansheng Road, Beibei, Chongqing 400715, PR China;2. Food and Pharmaceutical Engineering Institute, Guiyang University, Guiyang, Guizhou 550005, PR China;3. Laboratory of Quality & Safety Risk Assessment for Agro-products on Storage and Preservation (Chongqing), Ministry of Agriculture and Rural Affairs of the People''s Republic of China, Chongqing 400715, PR China;4. Chinese-Hungarian Cooperative Research Centre for Food Science, Chongqing 400715, PR China;1. China Light Industry Key Laboratory of Meat Microbial Control and Utilization, Hefei University of Technology, Hefei 230009, Anhui Province, People''s Republic of China;2. Engineering Research Center of Bio-Process, Ministry of Education, Hefei University of Technology, Hefei 230009, Anhui Province, People''s Republic of China;3. School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, Anhui Province, People''s Republic of China |
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| Abstract: | Filling of the gastric lumen of rats with 1.0 M NaCl solution (5 ml) for 10 min under urethane anesthesia caused an increase in the gastric fluid concentrations of prostaglandin (PG) E2, 13, 14-dihydro-15-keto-PGE2 and 6-keto-PGF1α as determined by radioimmunoassay. PGE2 was the major PG generated. The levels of PGE2 in the gastric fluid were increased dose-dependently after filling the lumen with 0.3, 0.5, 0.7 or 1.0 M NaCl solutions. The pH of the gastric fluid increased similarly after 0.5 to 1.0 M NaCl solutions. Indomethacin (10 mg/kg, i.p.) suppressed the PGE2 increase caused by 1.0 M NaCl solution, but did not prevent the increase of the pH of the gastric fluid induced by intragastric 1.0 M NaCl. Infusion of tetragastrin (62.5 μg/kg/hr, i.v., for 10 min) caused a marked increase of acid secretion without modifying intragastic concentration of PGE2. The acid secretion due to tetragastrin was completely inhibited after intragastric administration of 1.0 M NaCl solution, while indomethacin restored the tetragastrin-induced acid secretion, with prevention of a rise of intragastric PGE2 levels. These observations suggest that 1.0 M NaCl solutions suppress basal intragastric acid through a mechanism which is independent of prostaglandins. In contrast, the suppression of tetragastrin-induced acid secretion by intragastric 1.0 M NaCl solution appears to be mediated through a release of prostaglandins |
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