Please use this identifier to cite or link to this item: http://nopr.niscpr.res.in/handle/123456789/4416
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dc.contributor.authorSandhiya, Selvarajan-
dc.contributor.authorDkhar, Steven Aibor-
dc.contributor.authorKrishna, Peddy Reddy Murali-
dc.contributor.authorRamaswamy, Subramanian-
dc.date.accessioned2009-06-01T12:12:48Z-
dc.date.available2009-06-01T12:12:48Z-
dc.date.issued2008-01-
dc.identifier.issn0019-5189-
dc.identifier.urihttp://hdl.handle.net/123456789/4416-
dc.description60-65en_US
dc.description.abstractProkinetic drugs like mosapride, domperidone etc, are used to treat gastrointestinal delay. Though the receptor-mediated actions of these agents have been studied, involvement of ion channels in reversing morphine-induced gastrointestinal inertia by prokinetic agents has not been explored. Charcoal meal test was used to measure small intestinal transit (SIT) in adult male Swiss albino mice. Animals were given ion channel modifiers and prokinetic drugs intragastrically. Reversal of morphine-induced gastrointestinal delay by mosapride was decreased significantly by CaCl2, minoxidil and glibenclamide. Similarly, domperidone’s effect on morphine was decreased by CaCl2, nifedipine, minoxidil and glibenclamide significantly. The results reveal that ion channel modifiers counteract the prokinetic effects of mosapride or domperidone.en_US
dc.language.isoen_USen_US
dc.publisherCSIRen_US
dc.sourceIJEB Vol.46(01) [January 2008]en_US
dc.subjectATP gated K+ channelsen_US
dc.subjectGastrointestinal delayen_US
dc.subjectIon channel modifiersen_US
dc.subject‘L’ type voltage gated calcium channelsen_US
dc.subjectMorphineen_US
dc.subjectProkinetic drugsen_US
dc.subjectSmall intestinal transiten_US
dc.titleRole of ion channel modifiers in reversal of morphine–induced gastrointestinal inertia by prokinetic agents in miceen_US
dc.typeArticleen_US
Appears in Collections:IJEB Vol.46(01) [January 2008]

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