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Article: Endothelium-dependent hyperpolarization of vascular smooth muscle cells

TitleEndothelium-dependent hyperpolarization of vascular smooth muscle cells
Authors
Issue Date2000
Citation
Acta Pharmacologica Sinica, 2000, v. 21 n. 1, p. 1-18 How to Cite?
AbstractIn response to various neurohumoral substances endothelial cells release nitric oxide (NO) and prostacyclin, and produce hyperpolarization of the underlying vascular smooth muscle cells, possibly by releasing another factor termed endothelium-derived hyperpolarizing factor (EDHF). NO and prostacyclin stimulate smooth muscle soluble guanylate and adenylate cyclase respectively and can activate, depending on the vascular tissue studied, ATP-sensitive potassium (K(ATP)) and large conductance calcium-activated potassium channels (BK(Ca)). Furthermore, NO directly activates BK(Ca). In contrast to NO and prostacyclin, EDHF-mediated responses are sensitive to the combination of charybdotoxin plus apamin but do not involve K(ATP) or BK(Ca). As hyperpolarization of the endothelial cells is required to observe endothelium-dependent hyperpolarization, an electric coupling through myoendothelial 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. Therefore, in some vascular tissue K+ could be EDHF. Endothelial cells produce metabolites of the cytochrome P450-monooxygenase that activate BK(Ca), and induce hyperpolarization of coronary arterial smooth muscle cells. Whether or not EDHF could be an epoxyeicosatrienoic acid is still a matter of debate. The elucidation of the mechanism underlying endothelium-dependent hyperpolarizations and the discovery of specific inhibitors of the phenomenon are prerequisite for the understanding of the physiologic role of this alternative endothelial pathway involved in the control of vascular tone in health and disease.
Persistent Identifierhttp://hdl.handle.net/10722/171306
ISSN
2000 Impact Factor: 0.485
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:17Z-
dc.date.available2012-10-30T06:13:17Z-
dc.date.issued2000en_US
dc.identifier.citationActa Pharmacologica Sinica, 2000, v. 21 n. 1, p. 1-18en_US
dc.identifier.issn0253-9756en_US
dc.identifier.urihttp://hdl.handle.net/10722/171306-
dc.description.abstractIn response to various neurohumoral substances endothelial cells release nitric oxide (NO) and prostacyclin, and produce hyperpolarization of the underlying vascular smooth muscle cells, possibly by releasing another factor termed endothelium-derived hyperpolarizing factor (EDHF). NO and prostacyclin stimulate smooth muscle soluble guanylate and adenylate cyclase respectively and can activate, depending on the vascular tissue studied, ATP-sensitive potassium (K(ATP)) and large conductance calcium-activated potassium channels (BK(Ca)). Furthermore, NO directly activates BK(Ca). In contrast to NO and prostacyclin, EDHF-mediated responses are sensitive to the combination of charybdotoxin plus apamin but do not involve K(ATP) or BK(Ca). As hyperpolarization of the endothelial cells is required to observe endothelium-dependent hyperpolarization, an electric coupling through myoendothelial 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. Therefore, in some vascular tissue K+ could be EDHF. Endothelial cells produce metabolites of the cytochrome P450-monooxygenase that activate BK(Ca), and induce hyperpolarization of coronary arterial smooth muscle cells. Whether or not EDHF could be an epoxyeicosatrienoic acid is still a matter of debate. The elucidation of the mechanism underlying endothelium-dependent hyperpolarizations and the discovery of specific inhibitors of the phenomenon are prerequisite for the understanding of the physiologic role of this alternative endothelial pathway involved in the control of vascular tone in health and disease.en_US
dc.languageengen_US
dc.relation.ispartofActa Pharmacologica Sinicaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Metabolism - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Cytology - Physiologyen_US
dc.subject.meshEpoprostenol - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Physiologyen_US
dc.subject.meshNitric Oxide - Pharmacologyen_US
dc.subject.meshPotassium Channels - Drug Effectsen_US
dc.titleEndothelium-dependent hyperpolarization of vascular smooth muscle cellsen_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.pmid11263241-
dc.identifier.scopuseid_2-s2.0-0343986272en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0343986272&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume21en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage18en_US
dc.identifier.isiWOS:000084710700001-
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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