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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
2013 Impact Factor: 2.496
 
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 FieldValue
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
2013 Impact Factor: 2.496
 
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
 
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Author Affiliations
  1. The University of Hong Kong