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Article: Endothelium-derived vasoactive factors and hypertension: Possible roles in pathogenesis and as treatment targets
Title | Endothelium-derived vasoactive factors and hypertension: Possible roles in pathogenesis and as treatment targets |
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Authors | |
Keywords | Calcium channels Cyclooxygenase Cytochrome P450 Monooxygenase End-organ damage Endothelial dysfunction Gap junctions Guanylyl cyclase Lipoxygenase NAD(P)H oxidase NO-synthase Oxidative stress Potassium channels Prostacyclin Thromboxane A2 TRP channels |
Issue Date | 2010 |
Publisher | Springer Healthcare. The Journal's web site is located at http://www.springerlink.com/content/1522-6417/ |
Citation | Current Hypertension Reports, 2010, v. 12 n. 4, p. 267-275 How to Cite? |
Abstract | Endothelial cells regulate vascular tone by releasing various contracting and relaxing factors including nitric oxide (NO), arachidonic acid metabolites (derived from cyclooxygenases, lipoxygenases, and cytochrome P450 monooxygenases), reactive oxygen species, and vasoactive peptides. Additionally, another pathway associated with the hyperpolarization of the underlying smooth muscle cells plays a predominant role in resistance arteries. Endothelial dysfunction is a multifaceted disorder, which has been associated with hypertension of diverse etiologies, involving not only alterations of the L-arginine NO-synthase-soluble guanylyl cyclase pathway but also reduced endothelium-dependent hyperpolarizations and enhanced production of contracting factors, particularly vasoconstrictor prostanoids. This brief review highlights these different endothelial pathways as potential drug targets for novel treatments in hypertension and the associated endothelial dysfunction and end-organ damage. © 2010 The .Author(s). |
Persistent Identifier | http://hdl.handle.net/10722/125259 |
ISSN | 2023 Impact Factor: 3.9 2023 SCImago Journal Rankings: 1.387 |
PubMed Central ID | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Félétou, M | en_HK |
dc.contributor.author | Köhler, R | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.date.accessioned | 2010-10-31T11:20:32Z | - |
dc.date.available | 2010-10-31T11:20:32Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Current Hypertension Reports, 2010, v. 12 n. 4, p. 267-275 | en_HK |
dc.identifier.issn | 1522-6417 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/125259 | - |
dc.description.abstract | Endothelial cells regulate vascular tone by releasing various contracting and relaxing factors including nitric oxide (NO), arachidonic acid metabolites (derived from cyclooxygenases, lipoxygenases, and cytochrome P450 monooxygenases), reactive oxygen species, and vasoactive peptides. Additionally, another pathway associated with the hyperpolarization of the underlying smooth muscle cells plays a predominant role in resistance arteries. Endothelial dysfunction is a multifaceted disorder, which has been associated with hypertension of diverse etiologies, involving not only alterations of the L-arginine NO-synthase-soluble guanylyl cyclase pathway but also reduced endothelium-dependent hyperpolarizations and enhanced production of contracting factors, particularly vasoconstrictor prostanoids. This brief review highlights these different endothelial pathways as potential drug targets for novel treatments in hypertension and the associated endothelial dysfunction and end-organ damage. © 2010 The .Author(s). | en_HK |
dc.language | eng | en_HK |
dc.publisher | Springer Healthcare. The Journal's web site is located at http://www.springerlink.com/content/1522-6417/ | en_HK |
dc.relation.ispartof | Current Hypertension Reports | en_HK |
dc.rights | The original publication is available at www.springerlink.com | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Calcium channels | en_HK |
dc.subject | Cyclooxygenase | en_HK |
dc.subject | Cytochrome P450 Monooxygenase | en_HK |
dc.subject | End-organ damage | en_HK |
dc.subject | Endothelial dysfunction | en_HK |
dc.subject | Gap junctions | en_HK |
dc.subject | Guanylyl cyclase | en_HK |
dc.subject | Lipoxygenase | en_HK |
dc.subject | NAD(P)H oxidase | en_HK |
dc.subject | NO-synthase | en_HK |
dc.subject | Oxidative stress | en_HK |
dc.subject | Potassium channels | en_HK |
dc.subject | Prostacyclin | en_HK |
dc.subject | Thromboxane A2 | en_HK |
dc.subject | TRP channels | en_HK |
dc.subject.mesh | Arachidonic Acid | - |
dc.subject.mesh | Calcium Channels | - |
dc.subject.mesh | Endothelium, Vascular - drug effects - enzymology - pathology | - |
dc.subject.mesh | Hypertension - enzymology - pathology | - |
dc.subject.mesh | Nitric Oxide Synthase - metabolism | - |
dc.title | Endothelium-derived vasoactive factors and hypertension: Possible roles in pathogenesis and as treatment targets | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1007/s11906-010-0118-2 | en_HK |
dc.identifier.pmid | 20532699 | - |
dc.identifier.pmcid | PMC2910890 | - |
dc.identifier.scopus | eid_2-s2.0-77956266974 | en_HK |
dc.identifier.hkuros | 175217 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-77956266974&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 12 | en_HK |
dc.identifier.issue | 4 | en_HK |
dc.identifier.spage | 267 | en_HK |
dc.identifier.epage | 275 | en_HK |
dc.identifier.isi | WOS:000283353600009 | - |
dc.publisher.place | United States | en_HK |
dc.description.other | Springer Open Choice, 01 Dec 2010 | - |
dc.identifier.scopusauthorid | Félétou, M=7006461826 | en_HK |
dc.identifier.scopusauthorid | Köhler, R=7201611491 | en_HK |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_HK |
dc.identifier.citeulike | 7298904 | - |
dc.identifier.issnl | 1522-6417 | - |