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- Publisher Website: 10.1007/s00424-010-0786-4
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- PMID: 20127126
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Article: Endothelial dysfunction: A strategic target in the treatment of hypertension?
Title | Endothelial dysfunction: A strategic target in the treatment of hypertension? |
---|---|
Authors | |
Keywords | Contraction Endothelium Free radical Hypertensive rats Prostaglandin |
Issue Date | 2010 |
Publisher | Springer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htm |
Citation | Pflugers Archiv European Journal Of Physiology, 2010, v. 459 n. 6, p. 995-1004 How to Cite? |
Abstract | Endothelial dysfunction is a common feature of hypertension, and it results from the imbalanced release of endothelium-derived relaxing factors (EDRFs; in particular, nitric oxide) and endothelium-derived contracting factors (EDCFs; angiotensin II, endothelins, uridine adenosine tetraphosphate, and cyclooxygenase-derived EDCFs). Thus, drugs that increase EDRFs (using direct nitric oxide releasing compounds, tetrahydrobiopterin, or l-arginine supplementation) or decrease EDCF release or actions (using cyclooxygenase inhibitor or thromboxane A2/prostanoid receptor antagonists) would prevent the dysfunction. Many conventional antihypertensive drugs, including angiotensin-converting enzyme inhibitors, calcium channel blockers, and third-generation β-blockers, possess the ability to reverse endothelial dysfunction. Their use is attractive, as they can address arterial blood pressure and vascular tone simultaneously. The severity of endothelial dysfunction correlates with the development of coronary artery disease and predicts future cardiovascular events. Thus, endothelial dysfunction needs to be considered as a strategic target in the treatment of hypertension. © 2010 Springer-Verlag. |
Persistent Identifier | http://hdl.handle.net/10722/139591 |
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 1.361 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tang, EHC | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.date.accessioned | 2011-09-23T05:52:19Z | - |
dc.date.available | 2011-09-23T05:52:19Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Pflugers Archiv European Journal Of Physiology, 2010, v. 459 n. 6, p. 995-1004 | en_HK |
dc.identifier.issn | 0031-6768 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/139591 | - |
dc.description.abstract | Endothelial dysfunction is a common feature of hypertension, and it results from the imbalanced release of endothelium-derived relaxing factors (EDRFs; in particular, nitric oxide) and endothelium-derived contracting factors (EDCFs; angiotensin II, endothelins, uridine adenosine tetraphosphate, and cyclooxygenase-derived EDCFs). Thus, drugs that increase EDRFs (using direct nitric oxide releasing compounds, tetrahydrobiopterin, or l-arginine supplementation) or decrease EDCF release or actions (using cyclooxygenase inhibitor or thromboxane A2/prostanoid receptor antagonists) would prevent the dysfunction. Many conventional antihypertensive drugs, including angiotensin-converting enzyme inhibitors, calcium channel blockers, and third-generation β-blockers, possess the ability to reverse endothelial dysfunction. Their use is attractive, as they can address arterial blood pressure and vascular tone simultaneously. The severity of endothelial dysfunction correlates with the development of coronary artery disease and predicts future cardiovascular events. Thus, endothelial dysfunction needs to be considered as a strategic target in the treatment of hypertension. © 2010 Springer-Verlag. | en_HK |
dc.language | eng | en_US |
dc.publisher | Springer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htm | en_HK |
dc.relation.ispartof | Pflugers Archiv European Journal of Physiology | en_HK |
dc.rights | The original publication is available at www.springerlink.com | - |
dc.subject | Contraction | en_HK |
dc.subject | Endothelium | en_HK |
dc.subject | Free radical | en_HK |
dc.subject | Hypertensive rats | en_HK |
dc.subject | Prostaglandin | en_HK |
dc.subject.mesh | Antihypertensive Agents - therapeutic use | - |
dc.subject.mesh | Endothelium, Vascular - physiopathology | - |
dc.subject.mesh | Hypertension - drug therapy - physiopathology | - |
dc.subject.mesh | Prostaglandin-Endoperoxide Synthases - metabolism | - |
dc.subject.mesh | Reactive Oxygen Species - metabolism | - |
dc.title | Endothelial dysfunction: A strategic target in the treatment of hypertension? | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Tang, EHC: evatang1@hku.hk | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.authority | Tang, EHC=rp01382 | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.description.nature | postprint | - |
dc.identifier.doi | 10.1007/s00424-010-0786-4 | en_HK |
dc.identifier.pmid | 20127126 | - |
dc.identifier.scopus | eid_2-s2.0-77952891127 | en_HK |
dc.identifier.hkuros | 192141 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-77952891127&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 459 | en_HK |
dc.identifier.issue | 6 | en_HK |
dc.identifier.spage | 995 | en_HK |
dc.identifier.epage | 1004 | en_HK |
dc.identifier.eissn | 1432-2013 | - |
dc.identifier.isi | WOS:000277376200019 | - |
dc.publisher.place | Germany | en_HK |
dc.identifier.scopusauthorid | Tang, EHC=9536518500 | en_HK |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_HK |
dc.identifier.citeulike | 6803434 | - |
dc.identifier.issnl | 0031-6768 | - |