Drugs online research references
Jpn J Pharmacol. 1988 Jan;46(1):35-42.
Difference between two isozymes of (Na+ + K+)-ATPase in the interaction with omeprazole.
Iwata H, Iwata C, Matsuda T.
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Osaka University, Japan.
The difference in functional SH groups between two isozymes (alpha(+) and alpha forms) of (Na+ + K+)-ATPase was examined using omeprazole, a hydrophobic drug which was reported to modify SH groups of gastric (H+ + K+)-ATPase. Omeprazole inhibited rat brain and kidney (Na+ + K+)-ATPase activities in a time- and dose-dependent manner, and it inhibited incorporation of [3H]NEM into the catalytic subunit of the enzymes. The inhibition was greater in the brain enzyme than in the kidney enzyme. The inhibition of the brain enzyme showed a lag time, whereas the kidney enzyme was inhibited according to pseudo-first order kinetics. The inhibition by omeprazole of Na+-dependent phosphorylation and K+-stimulated phosphatase activity in the brain enzyme preparation was parallel with that of the overall (Na+ + K+)-ATPase reaction, while the partial reactions of the kidney enzyme showed different sensitivities to inhibition by omeprazole. Furthermore, the inhibition by omeprazole of [3H]NEM reactivity in the brain alpha(+) form was greater in the presence of SDS than in the absence, whereas the inhibition in the brain and kidney alpha forms was less in the presence of SDS than in the absence. These findings suggest that the isozymes of (Na+ + K+)-ATPase differ in hydrophobicity of SH groups of their catalytic subunits.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2835535&dopt=Abstract
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Hepatogastroenterology. 1995 Jul-Aug;42(4):423-31.
Effect of hypergastrinemia and blockade of gastrin-receptors on pancreatic growth in the mouse.
Niederau C, Niederau M, Klonowski H, Luthen R, Ferrell LD.
Department of Medicine, Heinrich-Heine-University of Dusseldorf, Germany.
BACKGROUND/AIM: The present study evaluates whether endogenous gastrin regulates pancreatic growth in the mouse. MATERIALS AND METHODS: Male NMRI mice weighing 12-15 g were assigned to six groups (10 mice/group) which were treated with different combinations of 0.9% NaCl, omeprazole, a CCK-A antagonist, a CCK-B antagonist, loxiglumide, and L365, 260 for 10 days each according to different protocols. RESULTS: Omeprazole caused a marked, 10-fold increase in serum gastrin which was not affected by the gastrin antagonist, but markedly reduced by the CCK-A antagonist. The marked increase in endogenous gastrin caused by omeprazole did not promote pancreatic growth in any way. Similarly, the gastrin antagonist did not inhibit pancreatic growth. In contrast, the CCK-A antagonist significantly decreased pancreatic weight and protein content. CONCLUSIONS: The present results strongly suggest that endogenous gastrin--in contrast to CCK--does not regulate pancreatic growth in the mouse. The inhibitory effect of loxiglumide on omeprazole-induced increase in serum gastrin might be explained by recent findings which showed that CCK-A antagonists can stimulate gastric acid secretion probably due to a reduction of the inhibitory effect of basal CCK on the D-cell and its somatostatin release. Probably such a slight stimulation of gastric acid secretion caused by the CCK-A antagonist might reduce the gastrin increase caused by omeprazole's abolishment of acid secretion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8586382&dopt=Abstract
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Standard triple therapy remains an important option for eradicating Helicobacter pylori (Hp) in developing countries because of its relatively low cost. However, salvage therapies after failure of this regimen remain undefined. The authors therefore investigate the efficacy of 1-week quadruple therapy as a second-line treatment of Hp infection after failure of standard triple therapy. Seventy-eight patients who failed Hp eradication using a 2-week bismuth-based triple therapy were enrolled and received a course of 1-week quadruple therapy (lansoprazole, 30 mg twice daily; bismuth subcitrate, 120 mg four times daily; clarithromycin, 500 mg twice daily; and amoxicillin, 1,000 mg twice daily) as a salvage regimen. The Hp status was reassessed 7 weeks after cessation of therapy. Among the 78 patients, Hp eradication was achieved in 65 (83%, 95% confidence interval = 75-91%) by intention-to-treat analysis. Only five (6%) patients had side effects, and all (100%) showed good drug compliance. Multivariate analysis disclosed that coffee drinking was an independent factor for treatment failure (odds ratio = 5.3, 95% confidence interval = 1.2-23.6, p = 0.028). The authors therefore conclude that their 1-week quadruple therapy is an effective salvage regimen for Hp infection after failure of standard triple therapy in the population examined. The benefits of this regimen include the high eradication rate, the short duration of treatment, fewer side effects, and good drug compliance. Coffee consumption possibly is an important factor in failure of the rescue regimen. The mechanisms underlying the association between coffee drinking and eradication failure require further research.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11960067&dopt=Abstract
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