Drugs online research references
Br J Pharmacol. 2002 Mar;135(5):1292-6.
Protease-activated receptor-2 (PAR-2) in the rat gastric mucosa: immunolocalization and facilitation of pepsin/pepsinogen secretion.
Kawao N, Sakaguchi Y, Tagome A, Kuroda R, Nishida S, Irimajiri K, Nishikawa H, Kawai K, Hollenberg MD, Kawabata A.
School of Pharmaceutical Sciences, Kinki University, 3-4-1 Kowakae, Higashi-Osaka 577-8502, Japan.
1. Agonists of protease-activated receptor-2 (PAR-2) trigger neurally mediated mucus secretion accompanied by mucosal cytoprotection in the stomach. The present study immunolocalized PAR-2 in the rat gastric mucosa and examined if PAR-2 could modulate pepsin/pepsinogen secretion in rats. 2. PAR-2-like immunoreactivity was abundant in the deep regions of gastric mucosa, especially in chief cells. 3. The PAR-2 agonist SLIGRL-NH(2), but not the control peptide LSIGRL-NH(2), administered i.v. repeatedly at 0.3 - 1 micromol kg(-1), four times in total, significantly facilitated gastric pepsin secretion, although a single dose produced no significant effect. 4. The PAR-2-mediated gastric pepsin secretion was resistant to omeprazole, N(G)-nitro-L-arginine methyl ester (L-NAME) or atropine, and also to ablation of sensory neurons by capsaicin. 5. Our study thus provides novel evidence that PAR-2 is localized in mucosal chief cells and facilitates gastric pepsin secretion in the rats, most probably by a direct mechanism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11877338&dopt=Abstract
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Pharmacol Toxicol. 2001 Oct;89(4):208-13.
Effects of CCK2 receptor blockade on growth parameters in gastrointestinal tract and pancreas in rats.
Bjorkqvist M, Norlen P, Kitano M, Chen D, Zhao CM, de la Cour CD, Gagnemo-Persson C, Hakanson R.
Department of Physiological Sciences, University of Lund, Sweden.
Gastrin has a growth-promoting effect on the oxyntic mucosa of the stomach but has been claimed also to affect other parts of the gastrointestinal tract and pancreas. This report describes the effects of the cholecystokinin, (CCK2) receptor antagonists YM022 and YF476 on various growth parameters in the gastrointestinal tract and pancreas of the rat. YM022 and YF476 were given subcutaneously in doses known to produce maximum and sustained CCK2 receptor blockade. The body weight was not affected. However, the oxyntic mucosal weight, thickness and protein and DNA contents were reduced by 15-20% already within 1-2 days and by about 30% after 4-8 weeks of CCK2 receptor blockade. Hence, the response of the oxyntic mucosa to CCK2 receptor blockade was in the form of hypotrophy (reduced protein content) and hypoplasia (reduced DNA content). There were no obvious effects of CCK2 receptor blockade on the intestine or pancreas (nor on liver, kidney or thyroid). The proton pump inhibitor omeprazole was used to induce hypergastrinaemia and was given with or without YM022. Omeprazole treatment for 4 weeks increased the oxyntic mucosal weight and thickness by 15-20%. YM022 prevented these effects. We conclude that while elevated circulating gastrin levels, acting on CCK2 receptors, exert a growth-promoting effect on the oxyntic mucosa (but not elsewhere), normal serum gastrin levels exert a mucosa-preserving effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11881972&dopt=Abstract
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Helicobacter. 2002 Feb;7(1):1-8.
Critical effect of Helicobacter pylori infection on the effectiveness of omeprazole for prevention of gastric or duodenal ulcers among chronic NSAID users.
Graham DY.
Department of Medicine, Veterans Affairs Medical Center, Baylor College of Medicine, Houston, TX 77030, USA.
BACKGROUND: The recently reported OMNIUM and ASTRONAUT NSAID ulcer prevention trials using omeprazole to prevent endoscopic ulcer recurrence among chronic NSAID users suggested superiority over misoprostol or ranitidine. AIM: To test the hypothesis the results from the OMNIUM and ASTRONAUT studies would not be generalizible as ulcer healing and ulcer recurrence would differ in relation to Helicobacter pylori status. METHODS: The data regarding H. pylori status were made available by AstraZenca allowing separate analysis of the outcome of those with NSAID ulcers (i.e. without H. pylori infection) and those NSAID use was complicated with the presence of an active H. pylori infection. RESULTS: Reanalysis confirmed that omeprazole was superior to placebo for the prevention of ulcer recurrence in chronic NSAID users. However, overall omeprazole was not significantly better than the subtherapeutic dose (400 microg/day) of misoprostol (14.5% vs. 19.6%, respectively, p =.93); 400 microg of misoprostol was actually superior to omeprazole for the prevention of gastric ulcers among those NSAID ulcers (8.2% vs. 16.6% for misoprostol and omeprazole, respectively; p <.05). Omeprazole was also not statistically different from misoprostol for gastric ulcer prevention in those whose NSAID use was complicated by an active H. pylori infection. Omeprazole was not significantly different from 300 mg of ranitidine for the prevention of NSAID gastric ulcers (14.6% vs. 11.6%, respectively, p =.56). Duodenal ulcers were over represented among H. pylori infected NSAID users and duodenal ulcer prevention was more sensitive to acid suppression than gastric ulcer. CONCLUSION: The OMNIUM and ASTRONAUT trials may have provided an unrealistic sense of security regarding the effectiveness of omeprazole for protection against ulcer recurrence in chronic NSAID users.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11886469&dopt=Abstract
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