File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Scopus: eid_2-s2.0-0343986272
- PMID: 11263241
- WOS: WOS:000084710700001
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Endothelium-dependent hyperpolarization of vascular smooth muscle cells
Title | Endothelium-dependent hyperpolarization of vascular smooth muscle cells |
---|---|
Authors | |
Keywords | Arachidonic acid Cytochrome P-450 Electrophysiology Epoprostenol Gap junctions Hyperpolarization Nitric oxide Potassium channels Vascular endothelium Vascular smooth muscle |
Issue Date | 2000 |
Citation | Acta Pharmacologica Sinica, 2000, v. 21 n. 1, p. 1-18 How to Cite? |
Abstract | In 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 Identifier | http://hdl.handle.net/10722/171306 |
ISSN | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Félétou, M | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:13:17Z | - |
dc.date.available | 2012-10-30T06:13:17Z | - |
dc.date.issued | 2000 | en_US |
dc.identifier.citation | Acta Pharmacologica Sinica, 2000, v. 21 n. 1, p. 1-18 | en_US |
dc.identifier.issn | 0253-9756 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171306 | - |
dc.description.abstract | In 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.language | eng | en_US |
dc.relation.ispartof | Acta Pharmacologica Sinica | en_US |
dc.subject | Arachidonic acid | - |
dc.subject | Cytochrome P-450 | - |
dc.subject | Electrophysiology | - |
dc.subject | Epoprostenol | - |
dc.subject | Gap junctions | - |
dc.subject | Hyperpolarization | - |
dc.subject | Nitric oxide | - |
dc.subject | Potassium channels | - |
dc.subject | Vascular endothelium | - |
dc.subject | Vascular smooth muscle | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Biological Factors - Metabolism - Physiology | en_US |
dc.subject.mesh | Endothelium, Vascular - Cytology - Physiology | en_US |
dc.subject.mesh | Epoprostenol - Pharmacology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Membrane Potentials - Drug Effects | en_US |
dc.subject.mesh | Muscle Relaxation - Drug Effects | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular - Cytology - Physiology | en_US |
dc.subject.mesh | Nitric Oxide - Pharmacology | en_US |
dc.subject.mesh | Potassium Channels - Drug Effects | en_US |
dc.title | Endothelium-dependent hyperpolarization of vascular smooth muscle cells | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 11263241 | - |
dc.identifier.scopus | eid_2-s2.0-0343986272 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0343986272&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 21 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 1 | en_US |
dc.identifier.epage | 18 | en_US |
dc.identifier.isi | WOS:000084710700001 | - |
dc.identifier.scopusauthorid | Félétou, M=7006461826 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0253-9756 | - |