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Conference Paper: Lactic-acid-induced ATP release from rat skeletal muscular L6 cells is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) channels

TitleLactic-acid-induced ATP release from rat skeletal muscular L6 cells is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) channels
Authors
KeywordsCardiovascular disease
Issue Date2008
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
The 12th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM 2008), Faculty of Medicine, the University of Hong Kong, Hong Kong, China, 13-14 December 2008. In Journal of the Hong Kong College of Cardiology, 2008, v. 16 n. 2, p. 65, abstract no. P8 How to Cite?
AbstractBACKGROUND AND OBJECTIVE: We had previously shown that lactic-acidinfusion increased the interstitial ATP concentration of perfused rat skeletal muscle in-vivo, which could be inhibited by CFTRinh-172, a specific inhibitor of CFTR. A stable rat skeletal muscular L6 cell line was used in this study to confirm that skeletal muscle cells (rather than nerve or vascular cells) were responsible for the acidosis-induced ATP release; the role of CFTR in mediating the ATP efflux during lactic acid incubation was confirmed using …
DescriptionThis journal issue is proceedings of ICSM 2008
Poster Session
Persistent Identifierhttp://hdl.handle.net/10722/140566
ISSN
2020 SCImago Journal Rankings: 0.105

 

DC FieldValueLanguage
dc.contributor.authorTu, Jen_US
dc.contributor.authorBallard, HJen_US
dc.date.accessioned2011-09-23T06:14:27Z-
dc.date.available2011-09-23T06:14:27Z-
dc.date.issued2008en_US
dc.identifier.citationThe 12th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM 2008), Faculty of Medicine, the University of Hong Kong, Hong Kong, China, 13-14 December 2008. In Journal of the Hong Kong College of Cardiology, 2008, v. 16 n. 2, p. 65, abstract no. P8en_US
dc.identifier.issn1027-7811en_US
dc.identifier.urihttp://hdl.handle.net/10722/140566-
dc.descriptionThis journal issue is proceedings of ICSM 2008-
dc.descriptionPoster Session-
dc.description.abstractBACKGROUND AND OBJECTIVE: We had previously shown that lactic-acidinfusion increased the interstitial ATP concentration of perfused rat skeletal muscle in-vivo, which could be inhibited by CFTRinh-172, a specific inhibitor of CFTR. A stable rat skeletal muscular L6 cell line was used in this study to confirm that skeletal muscle cells (rather than nerve or vascular cells) were responsible for the acidosis-induced ATP release; the role of CFTR in mediating the ATP efflux during lactic acid incubation was confirmed using …-
dc.languageengen_US
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3en_US
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_US
dc.subjectCardiovascular disease-
dc.titleLactic-acid-induced ATP release from rat skeletal muscular L6 cells is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) channelsen_US
dc.typeConference_Paperen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1027-7811&volume=16&issue=2&spage=65&epage=&date=2008&atitle=Lactic-acid-induced+ATP+release+from+rat+skeletal+muscular+L6+cells+is+mediated+by+cystic+fibrosis+transmembrane+conductance+regulator+(CFTR)+channelsen_US
dc.identifier.emailBallard, HJ: ballard@hkucc.hku.hken_US
dc.identifier.authorityBallard, HJ=rp00367en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros196066en_US
dc.identifier.volume16en_US
dc.identifier.issue2-
dc.identifier.spage65, abstract no. P8en_US
dc.identifier.epage65, abstract no. P8en_US
dc.publisher.placeHong Kong-
dc.description.otherThe 12th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), Faculty of Medicine, the University of Hong Kong, Hong Kong, China, 13-14 December 2008. In Journal of the Hong Kong College of Cardiology, 2008, v. 16 n. 2, p. 65, abstract no. P8-
dc.identifier.issnl1027-7811-

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