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Article: Hyperpolarization as a mechanism for endothelium-dependent relaxations in the porcine coronary artery

TitleHyperpolarization as a mechanism for endothelium-dependent relaxations in the porcine coronary artery
Authors
Issue Date1992
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1992, v. 445, p. 355-367 How to Cite?
Abstract1. The nature of endothelium-dependent relaxations resistant to nitro-L-arginine was investigated in porcine coronary arteries by measuring isometric force and membrane potential in the presence of indomethacin. 2. Bradykinin induced concentration- and endothelium-dependent relaxations and hyperpolarization in tissues contracted with prostaglandin F(2α). Nitro-L-arginine did not affect either the relaxations or the hyperpolarization induced by bradykinin. The threshold concentration of bradykinin was the same for the nitro-L-arginine-resistant relaxations and the membrane hyperpolarization. 3. Nitro-L-arginine-resistant relaxations were evoked by several agents (A23187, thrombin and UK 14304) in addition to bradykinin. The amplitude of membrane hyperpolarizations observed with all agents was proportional to that of nitro-L-arginine-resistant relaxations. 4. Thrombin caused more transient relaxations and hyperpolarizations than bradykinin the presence of nitro-L-arginine. 5. In tissues contracted with high K+ or tetrabutylammonium (a non-selective K+-channel blocker), bradykinin inhibited the contractions in a concentration-dependent manner, whereas membrane hyperpolarization was not observed. The relaxations evoked by the kinin were abolished by nitro-L-arginine. 6. These results suggest that endothelium-dependent relaxations which are resistant to nitro-L-arginine are mediated by membrane hyperpolarization in the porcine coronary artery.
Persistent Identifierhttp://hdl.handle.net/10722/171051
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNagao, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:59Z-
dc.date.available2012-10-30T06:11:59Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Physiology, 1992, v. 445, p. 355-367en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/171051-
dc.description.abstract1. The nature of endothelium-dependent relaxations resistant to nitro-L-arginine was investigated in porcine coronary arteries by measuring isometric force and membrane potential in the presence of indomethacin. 2. Bradykinin induced concentration- and endothelium-dependent relaxations and hyperpolarization in tissues contracted with prostaglandin F(2α). Nitro-L-arginine did not affect either the relaxations or the hyperpolarization induced by bradykinin. The threshold concentration of bradykinin was the same for the nitro-L-arginine-resistant relaxations and the membrane hyperpolarization. 3. Nitro-L-arginine-resistant relaxations were evoked by several agents (A23187, thrombin and UK 14304) in addition to bradykinin. The amplitude of membrane hyperpolarizations observed with all agents was proportional to that of nitro-L-arginine-resistant relaxations. 4. Thrombin caused more transient relaxations and hyperpolarizations than bradykinin the presence of nitro-L-arginine. 5. In tissues contracted with high K+ or tetrabutylammonium (a non-selective K+-channel blocker), bradykinin inhibited the contractions in a concentration-dependent manner, whereas membrane hyperpolarization was not observed. The relaxations evoked by the kinin were abolished by nitro-L-arginine. 6. These results suggest that endothelium-dependent relaxations which are resistant to nitro-L-arginine are mediated by membrane hyperpolarization in the porcine coronary artery.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsometric Contraction - Drug Effectsen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshQuinoxalines - Pharmacologyen_US
dc.subject.meshThrombin - Pharmacologyen_US
dc.subject.meshVasodilation - Physiologyen_US
dc.titleHyperpolarization as a mechanism for endothelium-dependent relaxations in the 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.pmid1501139-
dc.identifier.scopuseid_2-s2.0-0026567210en_US
dc.identifier.volume445en_US
dc.identifier.spage355en_US
dc.identifier.epage367en_US
dc.identifier.isiWOS:A1992HA11500020-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridNagao, T=7401489430en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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