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Conference Paper: The alternative: EDHF

TitleThe alternative: EDHF
Authors
Issue Date1999
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 1999, v. 31 n. 1, p. 15-22 How to Cite?
AbstractEndothelium-dependent relaxations cannot be fully explained by the release of either NO or/and prostacyclin. Another unidentified substance(s) which hyperpolarizes the underlying vascular smooth muscle cells may contribute to endothelium-dependent relaxations, especially in small arteries. It has been termed endothelium-derived hyperpolarizing factor (EDHF). In blood vessels from various species including humans, endothelium-dependent relaxations are partially or totally resistant to inhibitors of NO synthase and cyclooxygenase and are observed without an increase in the intracellular level of cyclic nucleotides in the vascular smooth muscle cells. In some species (canine, porcine and human) nitrovasodilators do not cause hyperpolarization while in other (rat, guinea-pig, rabbit), they evoke glibenclamide-sensitive hyperpolarization, suggesting the involvement of ATP-dependent potassium channels. In contrast, hyperpolarizations caused by EDHF are insensitive to glibenclamide but are inhibited by apamin or the combination of charybdotoxin plus apamin, indicating that NO and EDHF interact with two different targets. The existence of EDHF as a diffusable substance has been demonstrated under bioassay conditions whereby the source of EDHF was either native vascular segments or cultured endothelial cells. The identification of EDHF may allow a better understanding of its physiological and pathophysiological role(s).
Persistent Identifierhttp://hdl.handle.net/10722/173537
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFeletou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:33Z-
dc.date.available2012-10-30T06:32:33Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 1999, v. 31 n. 1, p. 15-22en_US
dc.identifier.issn0022-2828en_US
dc.identifier.urihttp://hdl.handle.net/10722/173537-
dc.description.abstractEndothelium-dependent relaxations cannot be fully explained by the release of either NO or/and prostacyclin. Another unidentified substance(s) which hyperpolarizes the underlying vascular smooth muscle cells may contribute to endothelium-dependent relaxations, especially in small arteries. It has been termed endothelium-derived hyperpolarizing factor (EDHF). In blood vessels from various species including humans, endothelium-dependent relaxations are partially or totally resistant to inhibitors of NO synthase and cyclooxygenase and are observed without an increase in the intracellular level of cyclic nucleotides in the vascular smooth muscle cells. In some species (canine, porcine and human) nitrovasodilators do not cause hyperpolarization while in other (rat, guinea-pig, rabbit), they evoke glibenclamide-sensitive hyperpolarization, suggesting the involvement of ATP-dependent potassium channels. In contrast, hyperpolarizations caused by EDHF are insensitive to glibenclamide but are inhibited by apamin or the combination of charybdotoxin plus apamin, indicating that NO and EDHF interact with two different targets. The existence of EDHF as a diffusable substance has been demonstrated under bioassay conditions whereby the source of EDHF was either native vascular segments or cultured endothelial cells. The identification of EDHF may allow a better understanding of its physiological and pathophysiological role(s).en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_US
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Biosynthesis - Physiologyen_US
dc.subject.meshBlood Vessels - Metabolismen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMuscle, Smooth, Vascular - Metabolismen_US
dc.subject.meshPotassium - Metabolismen_US
dc.titleThe alternative: EDHFen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1006/jmcc.1998.0840en_US
dc.identifier.pmid10072712-
dc.identifier.scopuseid_2-s2.0-0033059086en_US
dc.identifier.volume31en_US
dc.identifier.issue1en_US
dc.identifier.spage15en_US
dc.identifier.epage22en_US
dc.identifier.isiWOS:000078427700003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridFeletou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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