File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1152/ajpheart.00292.2006
- Scopus: eid_2-s2.0-33748421398
- PMID: 16632549
- WOS: WOS:000239680000001
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Endothelial dysfunction: A multifaceted disorder
Title | Endothelial dysfunction: A multifaceted disorder |
---|---|
Authors | |
Keywords | Angioplasty Endothelin Endothelium-derived contracting factor Endothelium-derived hperpolarizing factor Hypertension Nitric oxide Oxidative stress Prostaglandins Regenerated endothelium Superoxide anion |
Issue Date | 2006 |
Publisher | American Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/ |
Citation | American Journal Of Physiology - Heart And Circulatory Physiology, 2006, v. 291 n. 3, p. H985-H1002 How to Cite? |
Abstract | Endothelial cells synthesize and release various factors that regulate angiogenesis, inflammatory responses, hemostasis, as well as vascular tone and permeability. Endothelial dysfunction has been associated with a number of pathophysiological processes. Oxidative stress appears to be a common denominator underlying endothelial dysfunction in cardiovascular diseases. However, depending on the pathology, the vascular bed studied, the stimulant, and additional factors such as age, sex, salt intake, cholesterolemia, glycemia, and hyperhomocysteinemia, the mechanisms underlying the endothelial dysfunction can be markedly different. A reduced bioavailability of nitric oxide (NO), an alteration in the production of prostanoids, including prostacyclin, thromboxane A 2, and/or isoprostanes, an impairment of endothelium-dependent hyperpolarization, as well as an increased release of endothelin-1, can individually or in association contribute to endothelial dysfunction. Therapeutic interventions do not necessarily restore a proper endothelial function and, when they do, may improve only part of these variables. Copyright © 2006 the American Physiological Society. |
Persistent Identifier | http://hdl.handle.net/10722/80232 |
ISSN | 2023 Impact Factor: 4.1 2023 SCImago Journal Rankings: 1.452 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Félétou, M | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.date.accessioned | 2010-09-06T08:04:00Z | - |
dc.date.available | 2010-09-06T08:04:00Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | American Journal Of Physiology - Heart And Circulatory Physiology, 2006, v. 291 n. 3, p. H985-H1002 | en_HK |
dc.identifier.issn | 0363-6135 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/80232 | - |
dc.description.abstract | Endothelial cells synthesize and release various factors that regulate angiogenesis, inflammatory responses, hemostasis, as well as vascular tone and permeability. Endothelial dysfunction has been associated with a number of pathophysiological processes. Oxidative stress appears to be a common denominator underlying endothelial dysfunction in cardiovascular diseases. However, depending on the pathology, the vascular bed studied, the stimulant, and additional factors such as age, sex, salt intake, cholesterolemia, glycemia, and hyperhomocysteinemia, the mechanisms underlying the endothelial dysfunction can be markedly different. A reduced bioavailability of nitric oxide (NO), an alteration in the production of prostanoids, including prostacyclin, thromboxane A 2, and/or isoprostanes, an impairment of endothelium-dependent hyperpolarization, as well as an increased release of endothelin-1, can individually or in association contribute to endothelial dysfunction. Therapeutic interventions do not necessarily restore a proper endothelial function and, when they do, may improve only part of these variables. Copyright © 2006 the American Physiological Society. | en_HK |
dc.language | eng | en_HK |
dc.publisher | American Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/ | en_HK |
dc.relation.ispartof | American Journal of Physiology - Heart and Circulatory Physiology | en_HK |
dc.subject | Angioplasty | en_HK |
dc.subject | Endothelin | en_HK |
dc.subject | Endothelium-derived contracting factor | en_HK |
dc.subject | Endothelium-derived hperpolarizing factor | en_HK |
dc.subject | Hypertension | en_HK |
dc.subject | Nitric oxide | en_HK |
dc.subject | Oxidative stress | en_HK |
dc.subject | Prostaglandins | en_HK |
dc.subject | Regenerated endothelium | en_HK |
dc.subject | Superoxide anion | en_HK |
dc.title | Endothelial dysfunction: A multifaceted disorder | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6135&volume=291&spage=H985&epage=H1002&date=2006&atitle=Endothelial+dysfunction:+a+multifaceted+disorder | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1152/ajpheart.00292.2006 | en_HK |
dc.identifier.pmid | 16632549 | - |
dc.identifier.scopus | eid_2-s2.0-33748421398 | en_HK |
dc.identifier.hkuros | 123430 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-33748421398&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 291 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | H985 | en_HK |
dc.identifier.epage | H1002 | en_HK |
dc.identifier.isi | WOS:000239680000001 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Félétou, M=7006461826 | en_HK |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_HK |
dc.identifier.issnl | 0363-6135 | - |