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dc.contributor.authorYamakura, T
dc.contributor.authorLewohl, JM
dc.contributor.authorHarris, A
dc.date.accessioned2006-07-10
dc.date.accessioned2014-04-30T23:54:50Z
dc.date.accessioned2017-03-02T00:13:57Z
dc.date.available2017-03-02T00:13:57Z
dc.date.issued2001
dc.date.modified2014-04-30T23:54:50Z
dc.identifier.issn0003-3022
dc.identifier.urihttp://hdl.handle.net/10072/58921
dc.description.abstractBackground: General anesthetics differentially affect various families of potassium channels, and some potassium channels are suggested to be potential targets for anesthetics and alcohols. Methods: The voltage-gated (ERG1, ELK1, and KCNQ2/3) and inwardly rectifying (GIRK1/2, GIRK1/4, GIRK2, IRK1, and ROMK1) potassium channels were expressed in Xenopus oocytes. Effects of volatile agents [halothane, isoflurane, enflurane, F3 (1-chloro-1,2,2-trifluorocyclobutane), and the structurally related nonimmobilizer F6 (1,2-dichlorohexafluoro-cyclobutane)], as well as intravenous (pentobarbital, propofol, etomidate, alphaxalone, ketamine), and gaseous (nitrous oxide) anesthetics and alcohols (ethanol and hexanol) on channel function were studied using a two-electrode voltage clamp. Results: ERG1, ELK1, and KCNQ2/3 channels were either inhibited slightly or unaffected by concentrations corresponding to twice the minimum alveolar concentrations or twice the anesthetic EC50 of volatile and intravenous anesthetics and alcohols. In contrast, G protein–coupled inwardly rectifying potassium (GIRK) channels were inhibited by volatile anesthetics but not by intravenous anesthetics. The neuronal-type GIRK1/2 channels were inhibited by 2 minimum alveolar concentrations of halothane or F3 by 45 and 81%, respectively, whereas the cardiac-type GIRK1/4 channels were inhibited only by F3. Conversely, IRK1 and ROMK1 channels were completely resistant to all anesthetics tested. Current responses of GIRK2 channels activated by μ-opioid receptors were also inhibited by halothane. Nitrous oxide (∼0.6 atmosphere) slightly but selectively potentiated GIRK channels. Results of chimeric and multiple amino acid mutations suggest that the region containing the transmembrane domains, but not the pore-forming domain, may be involved in determining differences in anesthetic sensitivity between GIRK and IRK channels. Conclusions: G protein–coupled inwardly rectifying potassium channels, especially those composed of GIRK2 subunits, were inhibited by clinical concentrations of volatile anesthetics. This action may be related to some side effects of these agents.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.publisher.placeUnited States
dc.publisher.urihttps://doi.org/10.1097/00000542-200107000-00025
dc.relation.ispartofpagefrom144
dc.relation.ispartofpageto153
dc.relation.ispartofjournalAnesthesiology
dc.relation.ispartofvolume95
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchcode3202
dc.titleDifferential effects of general anesthetics on G-protein coupled inwardly rectifying and other potassium channels
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codec1x
gro.facultyGriffith Health Faculty
gro.date.issued2001
gro.hasfulltextNo Full Text
gro.griffith.authorLewohl, Joanne M.


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