Article: Full-length article Endothelium-derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins

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TitleFull-length article Endothelium-derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins
AuthorsNg, KFJ1
Leung, SWS1
Man, RYK1
Vanhoutte, PM1
KeywordsEndothelium-derived hyperpolarizing factor
Gi/o protein
Pertussis toxin
Pig coronary artery
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
CitationActa Pharmacologica Sinica, 2008, v. 29 n. 12, p. 1419-1424 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1745-7254.2008.00905.x
AbstractAim: Endothelium-dependent relaxations to certain neurohumoral substances are mediated by pertussis toxin-sensitive Gi/o protein. Our experiments were designed to determine the role, if any, of pertussis toxin-sensitive G-proteins in relaxations attributed to endothelium-derived hyperpolarizing factor (EDHF). Methods: Pig coronary arterial rings with endothelia were suspended in organ chambers flled with Krebs-Ringer bicarbonate solution maintained at 37 °C and continuously aerated with 95%O2 and 5% CO2. Isometric tension was measured during contractions to prostaglandin F2α in the presence of indomethacin and NΩnitro-L-arginine methyl ester (L-NAME). Results: Thrombin, the thrombin receptor-activating peptide SFLLRN, bradykinin, substance P, and calcimycin produced dose-dependent relaxations. These relaxations were not inhibited by prior incubation with pertussis toxin, but were abolished upon the addition of charybdotoxin plus apamin. Relaxations to the α2-adrenergic agonist UK14304 and those to serotonin were abolished in the presence of indomethacin and L-NAME. Conclusion: Unlike nitric oxide-mediated relaxations, EDHF-mediated relaxations of pig coronary arteries do not involve pertussis toxin-sensitive pathways and are Gi/o protein independent.
ISSN1671-4083
2011 Impact Factor: 1.953
2011 SCImago Journal Rankings: 0.136
DOIhttp://dx.doi.org/10.1111/j.1745-7254.2008.00905.x
ISI Accession Number IDWOS:000261710300003
Funding AgencyGrant Number
University of Hong Kong21374077
Funding Information:

This study is supported in part by a CRCG grant from the University of Hong Kong (No 21374077) and in part by departmental funds.

ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorNg, KFJ
dc.contributor.authorLeung, SWS
dc.contributor.authorMan, RYK
dc.contributor.authorVanhoutte, PM
dc.date.accessioned2010-09-06T05:53:41Z
dc.date.available2010-09-06T05:53:41Z
dc.date.issued2008
dc.description.abstractAim: Endothelium-dependent relaxations to certain neurohumoral substances are mediated by pertussis toxin-sensitive Gi/o protein. Our experiments were designed to determine the role, if any, of pertussis toxin-sensitive G-proteins in relaxations attributed to endothelium-derived hyperpolarizing factor (EDHF). Methods: Pig coronary arterial rings with endothelia were suspended in organ chambers flled with Krebs-Ringer bicarbonate solution maintained at 37 °C and continuously aerated with 95%O2 and 5% CO2. Isometric tension was measured during contractions to prostaglandin F2α in the presence of indomethacin and NΩnitro-L-arginine methyl ester (L-NAME). Results: Thrombin, the thrombin receptor-activating peptide SFLLRN, bradykinin, substance P, and calcimycin produced dose-dependent relaxations. These relaxations were not inhibited by prior incubation with pertussis toxin, but were abolished upon the addition of charybdotoxin plus apamin. Relaxations to the α2-adrenergic agonist UK14304 and those to serotonin were abolished in the presence of indomethacin and L-NAME. Conclusion: Unlike nitric oxide-mediated relaxations, EDHF-mediated relaxations of pig coronary arteries do not involve pertussis toxin-sensitive pathways and are Gi/o protein independent.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationActa Pharmacologica Sinica, 2008, v. 29 n. 12, p. 1419-1424 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1745-7254.2008.00905.x
dc.identifier.citeulike3804483
dc.identifier.doihttp://dx.doi.org/10.1111/j.1745-7254.2008.00905.x
dc.identifier.epage1424
dc.identifier.hkuros168517
dc.identifier.isiWOS:000261710300003
Funding AgencyGrant Number
University of Hong Kong21374077
Funding Information:

This study is supported in part by a CRCG grant from the University of Hong Kong (No 21374077) and in part by departmental funds.

dc.identifier.issn1671-4083
2011 Impact Factor: 1.953
2011 SCImago Journal Rankings: 0.136
dc.identifier.issue12
dc.identifier.openurl
dc.identifier.pmid19026160
dc.identifier.scopuseid_2-s2.0-64549097688
dc.identifier.spage1419
dc.identifier.urihttp://hdl.handle.net/10722/67291
dc.identifier.volume29
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.meshBiological Factors - pharmacology
dc.subject.meshCoronary Vessels - drug effects - physiology
dc.subject.meshEndothelium-Dependent Relaxing Factors - pharmacology
dc.subject.meshGTP-Binding Protein alpha Subunits, Gi-Go - metabolism
dc.subject.meshMuscle Relaxation - drug effects
dc.subjectEndothelium-derived hyperpolarizing factor
dc.subjectGi/o protein
dc.subjectPertussis toxin
dc.subjectPig coronary artery
dc.titleFull-length article Endothelium-derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong