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Article: Further investigations into the endothelium-dependent hyperpolarizing effects of bradykinin and substance P in porcine coronary artery

TitleFurther investigations into the endothelium-dependent hyperpolarizing effects of bradykinin and substance P in porcine coronary artery
Authors
Issue Date2001
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, 2001, v. 133 n. 7, p. 1145-1153 How to Cite?
Abstract1. In porcine coronary arteries, smooth muscle hyperpolarizations produced by the nitric oxide donor, NOR-1, and the prostacyclin analogue, iloprost, were compared with those induced by substance P and bradykinin and attributed to the endothelium-derived hyperpolarizing factor (EDHF). 2. In the presence of 300 μM L-nitroarginine and 10 μM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 μM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected. 3. Hyperpolarizations produced by maximally-effective concentrations of NOR-1 and NS1619 were identical (to -65 mV). They were significantly less than those generated by either substance P or bradykinin (to approximately -80 mV) and were abolished by iberiotoxin 100 nM, a concentration which had essentially no effect on responses to substance P or bradykinin. 4. Incubation of segments of intact arteries for 16-22 h in bicarbonate-buffered Krebs solution had little effect on EDHF responses to substance P or bradykinin. In contrast, after incubation for this period of time in HEPES-buffered Tyrode solution or Krebs containing 10 mM HEPES the EDHF response to substance P was abolished and that to bradykinin was markedly reduced, The residual bradykinin-induced hyperpolarization following incubation in Tyrode solution was inhibited by iberiotoxin and by 10 μM 17-octadecynoic acid. 5. We conclude that substance P activates only the EDHF pathway in the presence of nitric oxide synthase and cyclo-oxygenase inhibitors. Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K + channels, activated only by bradykinin.
Persistent Identifierhttp://hdl.handle.net/10722/171258
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.authorFélétou, Men_US
dc.contributor.authorGardener, MJen_US
dc.contributor.authorGlen, CDen_US
dc.contributor.authorRichards, GRen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorWeston, AHen_US
dc.date.accessioned2012-10-30T06:13:00Z-
dc.date.available2012-10-30T06:13:00Z-
dc.date.issued2001en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2001, v. 133 n. 7, p. 1145-1153en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171258-
dc.description.abstract1. In porcine coronary arteries, smooth muscle hyperpolarizations produced by the nitric oxide donor, NOR-1, and the prostacyclin analogue, iloprost, were compared with those induced by substance P and bradykinin and attributed to the endothelium-derived hyperpolarizing factor (EDHF). 2. In the presence of 300 μM L-nitroarginine and 10 μM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 μM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected. 3. Hyperpolarizations produced by maximally-effective concentrations of NOR-1 and NS1619 were identical (to -65 mV). They were significantly less than those generated by either substance P or bradykinin (to approximately -80 mV) and were abolished by iberiotoxin 100 nM, a concentration which had essentially no effect on responses to substance P or bradykinin. 4. Incubation of segments of intact arteries for 16-22 h in bicarbonate-buffered Krebs solution had little effect on EDHF responses to substance P or bradykinin. In contrast, after incubation for this period of time in HEPES-buffered Tyrode solution or Krebs containing 10 mM HEPES the EDHF response to substance P was abolished and that to bradykinin was markedly reduced, The residual bradykinin-induced hyperpolarization following incubation in Tyrode solution was inhibited by iberiotoxin and by 10 μM 17-octadecynoic acid. 5. We conclude that substance P activates only the EDHF pathway in the presence of nitric oxide synthase and cyclo-oxygenase inhibitors. Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K + channels, activated only by bradykinin.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.meshAnimalsen_US
dc.subject.meshBicarbonates - Pharmacologyen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshBuffersen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshCromakalim - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshEpoprostenol - Pharmacologyen_US
dc.subject.meshGlyburide - Pharmacologyen_US
dc.subject.meshHepes - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsotonic Solutions - Pharmacologyen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshNitric Oxide Donors - Pharmacologyen_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshSodium Chloride - Pharmacologyen_US
dc.subject.meshSubstance P - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleFurther investigations into the endothelium-dependent hyperpolarizing effects of bradykinin and substance P in 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.0704157-
dc.identifier.pmid11487526-
dc.identifier.scopuseid_2-s2.0-0034884135en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034884135&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume133en_US
dc.identifier.issue7en_US
dc.identifier.spage1145en_US
dc.identifier.epage1153en_US
dc.identifier.isiWOS:000170427900025-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridGardener, MJ=6603795865en_US
dc.identifier.scopusauthoridGlen, CD=55216630400en_US
dc.identifier.scopusauthoridRichards, GR=7201583688en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US

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