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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Nandi, Jyotirmoy Das, Pratap K. Zinkievich, J. Michael Baltodano, Juan D. Levine, Robert A. |
| Description | Country affiliation: United States Author Affiliation: Nandi J ( Division of Gastroenterology, Department of Medicine, State University of New York, Upstate Medical University, Syracuse, New York 13210, USA. nandij@upstate.edu) |
| Abstract | 1. In the present study, we evaluated the role of cyclo-oxygenase (COX)-1 and COX-2 on gastric acid secretion in rabbit isolated parietal cells and gastric glands by examining [(14)C]-aminopyrine uptake, prostaglandin (PG) E(2) synthesis and COX-1, COX-2 and proton pump expression at baseline and after treatment with various concentrations of specific COX-1 (SC-560), COX-2 (5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methyl-sulphonyl)phenyl-2 (5H)-furanone; DFU) and non-specific COX (indomethacin) inhibitors. 2. In parietal cells, SC-560 and indomethacin, over the concentration range 10(-8) to 10(-4) mol/L, dose-dependently increased basal and 10(-4) mol/L histamine-stimulated aminopyrine uptake and inhibited PGE(2) synthesis, whereas DFU (10(-8) to 10(-5) mol/L) had no effect. However, at 10(-4) mol/L, DFU augmented histamine-stimulated aminopyrine uptake by 135% and inhibited PGE(2) synthesis by 39%, indicating an inhibition of COX-1 at this higher concentration. 3. The SC-560-, DFU- and indomethacin-induced augmentation of histamine-stimulated aminopyrine uptake was reduced to basal levels after 10(-5) mol/L lansoprazole treatment in parietal cells and gastric glands, whereas 10(-4) mol/L ranitidine only partially inhibited such augmentation. 4. Only COX-1 was detected in parietal cells. However, both COX-1 and COX-2 were expressed in gastric glands, with relative protein density of COX-1 being sixfold higher than that of COX-2. Protein levels of COX-1 in parietal cells and those of COX-1 and COX-2 in gastric glands remained unchanged, regardless of inhibitor treatment, either alone or with histamine. 5. Parietal cell proton pump expression was significantly enhanced by 10(-5) mol/L SC-560 and 10(-4) mol/L indomethacin (by 29 and 31%, respectively) and pump activity was enhanced by 61 and 65%, respectively. In contrast, 10(-5) mol/L DFU had no effect. 6. In conclusion, the data indicate that inhibition of COX-1- but not COX-2-derived PGE(2) synthesis is involved in augmentation of non-steroidal anti-inflammatory drug-induced gastric acid secretion in parietal cells by enhancing expression and activation of the proton pump. |
| File Format | HTM / HTML |
| ISSN | 03051870 |
| Issue Number | 2 |
| Volume Number | 36 |
| e-ISSN | 14401681 |
| Journal | Clinical and Experimental Pharmacology and Physiology |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 2009-02-01 |
| Publisher Place | Australia |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Physiology Discipline Pharmacology Cyclooxygenase 1 Physiology Cyclooxygenase 2 Cyclooxygenase Inhibitors Pharmacology Gastric Acid Secretion H(+)-k(+)-exchanging Atpase Biosynthesis Parietal Cells, Gastric Drug Effects Aminopyrine Metabolism Animals Cells, Cultured Dinoprostone Inhibitory Concentration 50 Male Enzymology Rabbits Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology Physiology (medical) Pharmacology |
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