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Article: Role of gap junctions and EETs in endothelium-dependent hyperpolarization of porcine coronary artery

TitleRole of gap junctions and EETs in endothelium-dependent hyperpolarization of porcine coronary artery
Authors
Issue Date2000
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2000, v. 129 n. 6, p. 1145-1154 How to Cite?
Abstract1. The effects of endothelium-derived hyperpolarizing factor (EDHF: elicited using substance P or bradykinin) were compared with those of 11,12-EET in pig coronary artery. Smooth muscle cells were usually impaled with microelectrodes through the adventitial surface. 2. Substance P (100 nM) and 11,12-EET (11,12-epoxyeicosatrienoic acid; 3 μM) hyperpolarized endothelial cells in intact arteries. These actions were unaffected by 100 nM iberiotoxin but were abolished by charybdotoxin plus apamin (each 100 nM). 3. Substance P (100 nM) and bradykinin (30 nM) hyperpolarized intact artery smooth muscle; Substance P had no effect after endothelium removal. 4. 11,12-EET hyperpolarized de-endothelialized vessels by 12.6 ± 0.3 mV, an effect abolished by 100 nM iberiotoxin. 11,12-EET hyperpolarized intact arteries by 18.6 ± 0.8 mV, an action reduced by iberiotoxin, which was ineffective against substance P. Hyperpolarizations to 11,12-EET and substance P were partially inhibited by 100 nM charybdotoxin and abolished by further addition of 100 nM apamin. 5. 30 μM barium plus 500 nM ouabain depolarized intact artery smooth muscle but responses to substance P and bradykinin were unchanged. 500 μM gap 27 markedly reduced hyperpolarizations to substance P and bradykinin which were abolished in the additional presence of barium plus ouabain. 6. Substance P-induced hyperpolarizations of smooth muscle cells immediately below the internal elastic lamina were unaffected by gap 27, even in the presence of barium plus ouabain. 7. In pig coronary artery, 11,12-EET is not EDHF. Smooth muscle hyperpolarizations attributed to 'EDHF' are initiated by endothelial cell hyperpolarization involving charybdotoxin- (but not iberiotoxin) and apamin-sensitive K + channels. This may spread electrotonically via myoendothelial gap junctions but the involvement of an unknown endothelial factor cannot be excluded.
Persistent Identifierhttp://hdl.handle.net/10722/171242
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEdwards, Gen_US
dc.contributor.authorThollon, Cen_US
dc.contributor.authorGardener, MJen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorVilaine, JPen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorWeston, AHen_US
dc.date.accessioned2012-10-30T06:12:54Z-
dc.date.available2012-10-30T06:12:54Z-
dc.date.issued2000en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2000, v. 129 n. 6, p. 1145-1154en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171242-
dc.description.abstract1. The effects of endothelium-derived hyperpolarizing factor (EDHF: elicited using substance P or bradykinin) were compared with those of 11,12-EET in pig coronary artery. Smooth muscle cells were usually impaled with microelectrodes through the adventitial surface. 2. Substance P (100 nM) and 11,12-EET (11,12-epoxyeicosatrienoic acid; 3 μM) hyperpolarized endothelial cells in intact arteries. These actions were unaffected by 100 nM iberiotoxin but were abolished by charybdotoxin plus apamin (each 100 nM). 3. Substance P (100 nM) and bradykinin (30 nM) hyperpolarized intact artery smooth muscle; Substance P had no effect after endothelium removal. 4. 11,12-EET hyperpolarized de-endothelialized vessels by 12.6 ± 0.3 mV, an effect abolished by 100 nM iberiotoxin. 11,12-EET hyperpolarized intact arteries by 18.6 ± 0.8 mV, an action reduced by iberiotoxin, which was ineffective against substance P. Hyperpolarizations to 11,12-EET and substance P were partially inhibited by 100 nM charybdotoxin and abolished by further addition of 100 nM apamin. 5. 30 μM barium plus 500 nM ouabain depolarized intact artery smooth muscle but responses to substance P and bradykinin were unchanged. 500 μM gap 27 markedly reduced hyperpolarizations to substance P and bradykinin which were abolished in the additional presence of barium plus ouabain. 6. Substance P-induced hyperpolarizations of smooth muscle cells immediately below the internal elastic lamina were unaffected by gap 27, even in the presence of barium plus ouabain. 7. In pig coronary artery, 11,12-EET is not EDHF. Smooth muscle hyperpolarizations attributed to 'EDHF' are initiated by endothelial cell hyperpolarization involving charybdotoxin- (but not iberiotoxin) and apamin-sensitive K + channels. This may spread electrotonically via myoendothelial gap junctions but the involvement of an unknown endothelial factor cannot be excluded.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.mesh8,11,14-Eicosatrienoic Acid - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBarium - Pharmacologyen_US
dc.subject.meshBiological Factors - Pharmacologyen_US
dc.subject.meshCharybdotoxin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGap Junctions - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMicroelectrodesen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Innervationen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshSubstance P - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.titleRole of gap junctions and EETs in endothelium-dependent hyperpolarization of porcine coronary arteryen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjp.0703188-
dc.identifier.pmid10725263-
dc.identifier.scopuseid_2-s2.0-0034061942en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034061942&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume129en_US
dc.identifier.issue6en_US
dc.identifier.spage1145en_US
dc.identifier.epage1154en_US
dc.identifier.isiWOS:000085876000013-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US
dc.identifier.scopusauthoridThollon, C=6602540205en_US
dc.identifier.scopusauthoridGardener, MJ=6603795865en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridVilaine, JP=7004617134en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US

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