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Article: Endothelium-derived vasoactive factors and hypertension: Possible roles in pathogenesis and as treatment targets

TitleEndothelium-derived vasoactive factors and hypertension: Possible roles in pathogenesis and as treatment targets
Authors
KeywordsCalcium 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 Date2010
PublisherSpringer 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?
AbstractEndothelial 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 Identifierhttp://hdl.handle.net/10722/125259
ISSN
2015 Impact Factor: 3.112
2015 SCImago Journal Rankings: 1.172
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorKöhler, Ren_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-10-31T11:20:32Z-
dc.date.available2010-10-31T11:20:32Z-
dc.date.issued2010en_HK
dc.identifier.citationCurrent Hypertension Reports, 2010, v. 12 n. 4, p. 267-275en_HK
dc.identifier.issn1522-6417en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125259-
dc.description.abstractEndothelial 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.languageengen_HK
dc.publisherSpringer Healthcare. The Journal's web site is located at http://www.springerlink.com/content/1522-6417/en_HK
dc.relation.ispartofCurrent Hypertension Reportsen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCalcium channelsen_HK
dc.subjectCyclooxygenaseen_HK
dc.subjectCytochrome P450 Monooxygenaseen_HK
dc.subjectEnd-organ damageen_HK
dc.subjectEndothelial dysfunctionen_HK
dc.subjectGap junctionsen_HK
dc.subjectGuanylyl cyclaseen_HK
dc.subjectLipoxygenaseen_HK
dc.subjectNAD(P)H oxidaseen_HK
dc.subjectNO-synthaseen_HK
dc.subjectOxidative stressen_HK
dc.subjectPotassium channelsen_HK
dc.subjectProstacyclinen_HK
dc.subjectThromboxane A2en_HK
dc.subjectTRP channelsen_HK
dc.subject.meshArachidonic Acid-
dc.subject.meshCalcium Channels-
dc.subject.meshEndothelium, Vascular - drug effects - enzymology - pathology-
dc.subject.meshHypertension - enzymology - pathology-
dc.subject.meshNitric Oxide Synthase - metabolism-
dc.titleEndothelium-derived vasoactive factors and hypertension: Possible roles in pathogenesis and as treatment targetsen_HK
dc.typeArticleen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1007/s11906-010-0118-2en_HK
dc.identifier.pmid20532699-
dc.identifier.pmcidPMC2910890-
dc.identifier.scopuseid_2-s2.0-77956266974en_HK
dc.identifier.hkuros175217en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956266974&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue4en_HK
dc.identifier.spage267en_HK
dc.identifier.epage275en_HK
dc.identifier.isiWOS:000283353600009-
dc.publisher.placeUnited Statesen_HK
dc.description.otherSpringer Open Choice, 01 Dec 2010-
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridKöhler, R=7201611491en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike7298904-

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