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Conference Paper: The third pathway: Endothelium-dependent hyperpolarization

TitleThe third pathway: Endothelium-dependent hyperpolarization
Authors
Issue Date1999
Citation
Journal Of Physiology And Pharmacology, 1999, v. 50 n. 4, p. 525-534 How to Cite?
AbstractIn response to various neurohumoral substances endothelial cells release nitric oxide (NO), prostacyclin and produce hyperpolarization of the underlying vascular smooth muscle cells, possibly by releasing another factor termed endothelium-derived hyperpolarizing factor (EDHF). EDHF-mediated responses are sensitive to the combination of two toxins, charybdotoxin plus apamin, but do not involve ATP-sensitive or large conductance calcium- activated potassium channels. As hyperpolarization of the endothelial cells is required in order to observe endothelium-dependent hyperpolarization, and electrical coupling through myo-endothelial gap junctions may explain the phenomenon. An alternative explanation is that the hyperpolarization of the endothelial cells causes an efflux of potassium that in turn activates the inwardly rectifying potassium conductance and the Na+/K+ pump of the smooth muscle cells. Endothelial cells produce metabolites of the cytochrome P450- monooxygenase that activate BK(Ca), and induce hyperpolarization of coronary arterial smooth muscle cells. The elucidation of the mechanism underlying endothelium-dependent hyperpolarization and the discovery of specific inhibitors of the phenomenon are prerequisite for the understanding of the physiological role of this alternative endothelial pathway involved in the control of vascular tone in health and disease.
Persistent Identifierhttp://hdl.handle.net/10722/173538
ISSN
2015 Impact Factor: 2.804
2015 SCImago Journal Rankings: 0.888
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, 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 Physiology And Pharmacology, 1999, v. 50 n. 4, p. 525-534en_US
dc.identifier.issn0867-5910en_US
dc.identifier.urihttp://hdl.handle.net/10722/173538-
dc.description.abstractIn response to various neurohumoral substances endothelial cells release nitric oxide (NO), prostacyclin and produce hyperpolarization of the underlying vascular smooth muscle cells, possibly by releasing another factor termed endothelium-derived hyperpolarizing factor (EDHF). EDHF-mediated responses are sensitive to the combination of two toxins, charybdotoxin plus apamin, but do not involve ATP-sensitive or large conductance calcium- activated potassium channels. As hyperpolarization of the endothelial cells is required in order to observe endothelium-dependent hyperpolarization, and electrical coupling through myo-endothelial gap junctions may explain the phenomenon. An alternative explanation is that the hyperpolarization of the endothelial cells causes an efflux of potassium that in turn activates the inwardly rectifying potassium conductance and the Na+/K+ pump of the smooth muscle cells. Endothelial cells produce metabolites of the cytochrome P450- monooxygenase that activate BK(Ca), and induce hyperpolarization of coronary arterial smooth muscle cells. The elucidation of the mechanism underlying endothelium-dependent hyperpolarization and the discovery of specific inhibitors of the phenomenon are prerequisite for the understanding of the physiological role of this alternative endothelial pathway involved in the control of vascular tone in health and disease.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Physiology and Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Secretionen_US
dc.subject.meshCytochrome P-450 Enzyme System - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshGap Junctions - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMembrane Potentials - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshPotassium Channels - Physiologyen_US
dc.titleThe third pathway: Endothelium-dependent hyperpolarizationen_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.pmid10639003-
dc.identifier.scopuseid_2-s2.0-0033377927en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033377927&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume50en_US
dc.identifier.issue4en_US
dc.identifier.spage525en_US
dc.identifier.epage534en_US
dc.identifier.isiWOS:000084398300005-
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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