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Article: Bradykinin-induced, endothelium-dependent responses in porcine coronary arteries: Involvement of potassium channel activation and epoxyeicosatrienoic acids

TitleBradykinin-induced, endothelium-dependent responses in porcine coronary arteries: Involvement of potassium channel activation and epoxyeicosatrienoic acids
Authors
Issue Date2005
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, 2005, v. 145 n. 6, p. 775-784 How to Cite?
AbstractIn coronary arteries, bradykinin opens endothelial intermediate- and small-conductance Ca 2+-sensitive K + channels (IK Ca and SK Ca) and, additionally, releases epoxyeicosatrienoic acids (EETs) from the endothelium. To clarify the involvement of these pathways in endothelium-dependent myocyte hyperpolarization, bradykinin-induced electrical changes in endothelial cells and myocytes of porcine coronary arteries (following nitric oxide (NO) synthase and cyclooxygenase inhibition) were measured using sharp microelectrodes. Hyperpolarization of endothelial cells by bradykinin (27.0±0.9 mV, n = 4) was partially inhibited (74%) by blockade of IK Ca and SK Ca channels using 10 μM TRAM-39 (2-(2-chlorophenyl)-2,2- diphenylacetonitrile) plus 100 nM apamin (leaving an iberiotoxin-sensitive component), whereas the response to substance P was abolished. After gap junction blockade with HEPES, (N-(2-hydroxyethyl)piperazine-N′-(2- ethanesulphonic acid)) hyperpolarization of the endothelium by 100 nM bradykinin was abolished by TRAM-39 plus apamin, whereas myocyte hyperpolarization still occurred (12.9 ± 1.0 mV, n = 4). The residual hyperpolarizations to 100 nM bradykinin were antagonized by the EET antagonist, 14,15-EEZE (14,15-epoxyeicosa-5(Z)-enoic acid) (10 μM), and abolished by iberiotoxin. Bradykinin-induced myocyte hyperpolarizations were also reduced by 14,15-EEZE-mSI (14,15-EEZE-methylsulfonylimide) (5,6- and 14,15-EET antagonist), whereas those to exogenous 11,12-EET were unaffected. These data show that bradykinin-induced hyperpolarization of endothelial cells (due to the opening of IK Ca and SK Ca channels) is electrotonically transferred to the myocytes via gap junctions. Bradykinin (but not substance P) also hyperpolarizes myocytes by a mechanism (independent of endothelial cell hyperpolarization) which involves endothelial cell production of EETs (most likely 14,15- and/or 11,12-EET). These open endothelial IK Ca and SK Ca channels and also activate large-conductance calcium-sensitive K + channels (BK Ca) on the surrounding myocytes. © 2005 Nature Publishing Group. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171333
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWeston, AHen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorFalck, JRen_US
dc.contributor.authorCampbell, WBen_US
dc.contributor.authorEdwards, Gen_US
dc.date.accessioned2012-10-30T06:13:27Z-
dc.date.available2012-10-30T06:13:27Z-
dc.date.issued2005en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2005, v. 145 n. 6, p. 775-784en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171333-
dc.description.abstractIn coronary arteries, bradykinin opens endothelial intermediate- and small-conductance Ca 2+-sensitive K + channels (IK Ca and SK Ca) and, additionally, releases epoxyeicosatrienoic acids (EETs) from the endothelium. To clarify the involvement of these pathways in endothelium-dependent myocyte hyperpolarization, bradykinin-induced electrical changes in endothelial cells and myocytes of porcine coronary arteries (following nitric oxide (NO) synthase and cyclooxygenase inhibition) were measured using sharp microelectrodes. Hyperpolarization of endothelial cells by bradykinin (27.0±0.9 mV, n = 4) was partially inhibited (74%) by blockade of IK Ca and SK Ca channels using 10 μM TRAM-39 (2-(2-chlorophenyl)-2,2- diphenylacetonitrile) plus 100 nM apamin (leaving an iberiotoxin-sensitive component), whereas the response to substance P was abolished. After gap junction blockade with HEPES, (N-(2-hydroxyethyl)piperazine-N′-(2- ethanesulphonic acid)) hyperpolarization of the endothelium by 100 nM bradykinin was abolished by TRAM-39 plus apamin, whereas myocyte hyperpolarization still occurred (12.9 ± 1.0 mV, n = 4). The residual hyperpolarizations to 100 nM bradykinin were antagonized by the EET antagonist, 14,15-EEZE (14,15-epoxyeicosa-5(Z)-enoic acid) (10 μM), and abolished by iberiotoxin. Bradykinin-induced myocyte hyperpolarizations were also reduced by 14,15-EEZE-mSI (14,15-EEZE-methylsulfonylimide) (5,6- and 14,15-EET antagonist), whereas those to exogenous 11,12-EET were unaffected. These data show that bradykinin-induced hyperpolarization of endothelial cells (due to the opening of IK Ca and SK Ca channels) is electrotonically transferred to the myocytes via gap junctions. Bradykinin (but not substance P) also hyperpolarizes myocytes by a mechanism (independent of endothelial cell hyperpolarization) which involves endothelial cell production of EETs (most likely 14,15- and/or 11,12-EET). These open endothelial IK Ca and SK Ca channels and also activate large-conductance calcium-sensitive K + channels (BK Ca) on the surrounding myocytes. © 2005 Nature Publishing Group. All rights reserved.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.meshAcetonitriles - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApamin - Pharmacologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshMuscle Cells - Drug Effects - Physiologyen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshPotassium Channel Blockers - Pharmacologyen_US
dc.subject.meshPotassium Channels, Calcium-Activated - Drug Effects - Metabolismen_US
dc.subject.meshReceptors, Eicosanoid - Antagonists & Inhibitorsen_US
dc.subject.meshSubstance P - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshTrityl Compounds - Pharmacologyen_US
dc.titleBradykinin-induced, endothelium-dependent responses in porcine coronary arteries: Involvement of potassium channel activation and epoxyeicosatrienoic acidsen_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.0706256en_US
dc.identifier.pmid15895105-
dc.identifier.scopuseid_2-s2.0-23044461193en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23044461193&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume145en_US
dc.identifier.issue6en_US
dc.identifier.spage775en_US
dc.identifier.epage784en_US
dc.identifier.isiWOS:000230588500010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridFalck, JR=7101749267en_US
dc.identifier.scopusauthoridCampbell, WB=7402860555en_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US

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