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Article: Endothelium-derived nitric oxide inhibits the relaxation of the porcine coronary artery to natriuretic peptides by desensitizing big conductance calcium-activated potassium channels of vascular smooth muscle

TitleEndothelium-derived nitric oxide inhibits the relaxation of the porcine coronary artery to natriuretic peptides by desensitizing big conductance calcium-activated potassium channels of vascular smooth muscle
Authors
Issue Date2010
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 2010, v. 334 n. 1, p. 223-231 How to Cite?
AbstractThe present experiments investigated whether endothelium-derived mediators modulate the effect of natriuretic peptides in porcine coronary arteries. Rings with and without endothelium were suspended in organ chambers for isometric tension recording. Concentration-relaxation curves to C-type natriuretic peptide (CNP) and atrial natriuretic peptide (ANP) were obtained during contractions to endothelin-1. Removal of the endothelium potentiated relaxations to both CNP and ANP. Nω-nitro-L-arginine methyl ester potentiated relaxations to natriuretic peptides only in arteries with endothelium. Sodium nitroprusside (SNP) inhibited the response to the natriuretic peptides only in the absence of the endothelium. In rings with endothelium, 1H-[1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (ODQ) and 4H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4] oxazin-1-one (NS2028) potentiated CNP-mediated relaxations. Iberiotoxin (IBTX) reduced the response only in rings without endothelium. Glybenclamide inhibited the relaxations in both the presence and absence of endothelium. CNP-induced relaxations were reduced by 8-bromoguanosine 3′,5′-cGMP (8-bromo-cGMP) to the same extent in rings with and without endothelium. There was no significant difference between the increased cGMP content caused by CNP in porcine coronary arteries with or without endothelium. In patch-clamp studies in porcine coronary arterial smooth muscle cells, the natriuretic peptide-mediated enhancement of the IBTX-sensitive big conductance calcium-activated potassium channel (BKCa) amplitude was reversed by SNP and 8-bromo-cGMP. These findings demonstrate that, in the porcine coronary artery, the opening of BKCa and ATP-dependent potassium channels of the vascular smooth muscle contributes to CNP-mediated relaxations. Endothelium-derived and exogenousNO inhibit the direct relaxing effect of natriuretic peptides by desensitizing the response of the BKCas of the vascular smooth muscle to the generation of cGMP. Copyright © 2010 by The American Society for Pharmacology and Experimental Therapeutics.
Persistent Identifierhttp://hdl.handle.net/10722/147275
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiang, CFen_HK
dc.contributor.authorAu, ALSen_HK
dc.contributor.authorLeung, SWSen_HK
dc.contributor.authorNg, KFJen_HK
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorKwan, YWen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2012-05-29T06:01:10Z-
dc.date.available2012-05-29T06:01:10Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 2010, v. 334 n. 1, p. 223-231en_HK
dc.identifier.issn0022-3565en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147275-
dc.description.abstractThe present experiments investigated whether endothelium-derived mediators modulate the effect of natriuretic peptides in porcine coronary arteries. Rings with and without endothelium were suspended in organ chambers for isometric tension recording. Concentration-relaxation curves to C-type natriuretic peptide (CNP) and atrial natriuretic peptide (ANP) were obtained during contractions to endothelin-1. Removal of the endothelium potentiated relaxations to both CNP and ANP. Nω-nitro-L-arginine methyl ester potentiated relaxations to natriuretic peptides only in arteries with endothelium. Sodium nitroprusside (SNP) inhibited the response to the natriuretic peptides only in the absence of the endothelium. In rings with endothelium, 1H-[1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (ODQ) and 4H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4] oxazin-1-one (NS2028) potentiated CNP-mediated relaxations. Iberiotoxin (IBTX) reduced the response only in rings without endothelium. Glybenclamide inhibited the relaxations in both the presence and absence of endothelium. CNP-induced relaxations were reduced by 8-bromoguanosine 3′,5′-cGMP (8-bromo-cGMP) to the same extent in rings with and without endothelium. There was no significant difference between the increased cGMP content caused by CNP in porcine coronary arteries with or without endothelium. In patch-clamp studies in porcine coronary arterial smooth muscle cells, the natriuretic peptide-mediated enhancement of the IBTX-sensitive big conductance calcium-activated potassium channel (BKCa) amplitude was reversed by SNP and 8-bromo-cGMP. These findings demonstrate that, in the porcine coronary artery, the opening of BKCa and ATP-dependent potassium channels of the vascular smooth muscle contributes to CNP-mediated relaxations. Endothelium-derived and exogenousNO inhibit the direct relaxing effect of natriuretic peptides by desensitizing the response of the BKCas of the vascular smooth muscle to the generation of cGMP. Copyright © 2010 by The American Society for Pharmacology and Experimental Therapeutics.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_HK
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshCyclic Gmp - Biosynthesisen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshGuanylate Cyclase - Antagonists & Inhibitorsen_US
dc.subject.meshIon Channel Gating - Drug Effectsen_US
dc.subject.meshLarge-Conductance Calcium-Activated Potassium Channels - Antagonists & Inhibitorsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshNatriuretic Peptides - Pharmacology - Physiologyen_US
dc.subject.meshNitric Oxide - Metabolism - Pharmacology - Physiologyen_US
dc.subject.meshNitric Oxide Donors - Pharmacologyen_US
dc.subject.meshOxadiazoles - Pharmacologyen_US
dc.subject.meshOxazines - Pharmacologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshVasodilation - Drug Effects - Physiologyen_US
dc.titleEndothelium-derived nitric oxide inhibits the relaxation of the porcine coronary artery to natriuretic peptides by desensitizing big conductance calcium-activated potassium channels of vascular smooth muscleen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, SWS: swsleung@hku.hken_HK
dc.identifier.emailNg, KFJ: jkfng@hkucc.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityLeung, SWS=rp00235en_HK
dc.identifier.authorityNg, KFJ=rp00544en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1124/jpet.110.166652en_HK
dc.identifier.pmid20332186en_HK
dc.identifier.scopuseid_2-s2.0-77953804779en_HK
dc.identifier.hkuros171115-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77953804779&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume334en_HK
dc.identifier.issue1en_HK
dc.identifier.spage223en_HK
dc.identifier.epage231en_HK
dc.identifier.isiWOS:000278901000025-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLiang, CF=36673425400en_HK
dc.identifier.scopusauthoridAu, ALS=7005391144en_HK
dc.identifier.scopusauthoridLeung, SWS=24540419500en_HK
dc.identifier.scopusauthoridNg, KFJ=13608809400en_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridKwan, YW=7005662153en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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