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Article: Potentiation of EDHF-mediated relaxation by chloride channel blockers
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TitlePotentiation of EDHF-mediated relaxation by chloride channel blockers
 
AuthorsYang, C2
Kwan, YW4
Chan, SW3
Lee, SMY1
Leung, GPH2
 
Keywordschloride channels
endothelium-derived hyperpolarizing factor
potassium channels
 
Issue Date2010
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
 
CitationActa Pharmacologica Sinica, 2010, v. 31 n. 10, p. 1303-1311 [How to Cite?]
DOI: http://dx.doi.org/10.1038/aps.2010.157
 
AbstractAim: To investigate the involvement of Cl channels in endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in rat mesenteric arteries. Methods: Cl channel and K ir channel activities were studied using whole-cell patch clamping in rat mesenteric arterial smooth muscle cells. Isometric tension of arterial rings was measured in organ chambers. Results: The volume-activated Cl current in rat mesenteric arterial smooth muscle cells was abolished by Cl channel blockers NPPB or DIDS. The EDHF-mediated vasorelaxation was potentiated by NPPB and DIDS. The EDHF response was diminished by a combination of apamin and charybdotoxin, which agreed with the hypothesis that EDHF response involves the release of K + via the Ca 2+-activated K + channels in endothelial cells. The elevation of K + concentration in bathing solution from 1.2 mmol/L to 11.2 mmol/L induced an arterial relaxation, which was abolished by the combination of BaCl 2 and ouabain. It is consistent to the hypothesis that K + activates K + /Na +-ATPase and inward rectifier K + (K ir) channels, leading to the hyperpolarization and relaxation of vascular smooth muscle. The K +-induced relaxation was augmented by NPPB, DIDS, or withdrawal of Cl from the bathing solution, which could be reversed by BaCl 2, but not ouabain. The potentiating effect of Cl channel blockers on K +-induced relaxation was probably due to the interaction between Cl channels and K ir channels. Moreover, the K +-induced relaxation was potentiated when the arteries were incubated in hyperosmotic solution, which is known to inhibit volume-activated Cl channels.Conclusion:The inhibition of Cl channels, particularly the volume-activated Cl channels, may potentiate the EDHF-induced vasorelaxation through the K ir channels. © 2010 CPS and SIMM All rights reserved.
 
ISSN1671-4083
2013 Impact Factor: 2.496
 
DOIhttp://dx.doi.org/10.1038/aps.2010.157
 
ISI Accession Number IDWOS:000283398200008
Funding AgencyGrant Number
Hong Kong SAR769607
University of Hong Kong
Funding Information:

This work was supported by the RGC Earmarked Grants of Hong Kong SAR (project code: 769607), and the Seed Funding for Basic Research Program of the University of Hong Kong.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYang, C
 
dc.contributor.authorKwan, YW
 
dc.contributor.authorChan, SW
 
dc.contributor.authorLee, SMY
 
dc.contributor.authorLeung, GPH
 
dc.date.accessioned2011-08-19T03:19:38Z
 
dc.date.available2011-08-19T03:19:38Z
 
dc.date.issued2010
 
dc.description.abstractAim: To investigate the involvement of Cl channels in endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in rat mesenteric arteries. Methods: Cl channel and K ir channel activities were studied using whole-cell patch clamping in rat mesenteric arterial smooth muscle cells. Isometric tension of arterial rings was measured in organ chambers. Results: The volume-activated Cl current in rat mesenteric arterial smooth muscle cells was abolished by Cl channel blockers NPPB or DIDS. The EDHF-mediated vasorelaxation was potentiated by NPPB and DIDS. The EDHF response was diminished by a combination of apamin and charybdotoxin, which agreed with the hypothesis that EDHF response involves the release of K + via the Ca 2+-activated K + channels in endothelial cells. The elevation of K + concentration in bathing solution from 1.2 mmol/L to 11.2 mmol/L induced an arterial relaxation, which was abolished by the combination of BaCl 2 and ouabain. It is consistent to the hypothesis that K + activates K + /Na +-ATPase and inward rectifier K + (K ir) channels, leading to the hyperpolarization and relaxation of vascular smooth muscle. The K +-induced relaxation was augmented by NPPB, DIDS, or withdrawal of Cl from the bathing solution, which could be reversed by BaCl 2, but not ouabain. The potentiating effect of Cl channel blockers on K +-induced relaxation was probably due to the interaction between Cl channels and K ir channels. Moreover, the K +-induced relaxation was potentiated when the arteries were incubated in hyperosmotic solution, which is known to inhibit volume-activated Cl channels.Conclusion:The inhibition of Cl channels, particularly the volume-activated Cl channels, may potentiate the EDHF-induced vasorelaxation through the K ir channels. © 2010 CPS and SIMM All rights reserved.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationActa Pharmacologica Sinica, 2010, v. 31 n. 10, p. 1303-1311 [How to Cite?]
DOI: http://dx.doi.org/10.1038/aps.2010.157
 
dc.identifier.doihttp://dx.doi.org/10.1038/aps.2010.157
 
dc.identifier.epage1311
 
dc.identifier.hkuros189176
 
dc.identifier.isiWOS:000283398200008
Funding AgencyGrant Number
Hong Kong SAR769607
University of Hong Kong
Funding Information:

This work was supported by the RGC Earmarked Grants of Hong Kong SAR (project code: 769607), and the Seed Funding for Basic Research Program of the University of Hong Kong.

 
dc.identifier.issn1671-4083
2013 Impact Factor: 2.496
 
dc.identifier.issue10
 
dc.identifier.openurl
 
dc.identifier.pmid20835269
 
dc.identifier.scopuseid_2-s2.0-77957735127
 
dc.identifier.spage1303
 
dc.identifier.urihttp://hdl.handle.net/10722/137119
 
dc.identifier.volume31
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
 
dc.publisher.placeUnited States
 
dc.relation.ispartofActa Pharmacologica Sinica
 
dc.relation.referencesReferences in Scopus
 
dc.subject.mesh4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology
 
dc.subject.meshChloride Channels - antagonists and inhibitors
 
dc.subject.meshEndothelium-Dependent Relaxing Factors - physiology
 
dc.subject.meshMesenteric Arteries - drug effects - physiology
 
dc.subject.meshNitrobenzoates - pharmacology
 
dc.subjectchloride channels
 
dc.subjectendothelium-derived hyperpolarizing factor
 
dc.subjectpotassium channels
 
dc.titlePotentiation of EDHF-mediated relaxation by chloride channel blockers
 
dc.typeArticle
 
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Author Affiliations
  1. University of Macau
  2. The University of Hong Kong
  3. Hong Kong Polytechnic University
  4. Chinese University of Hong Kong