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- Publisher Website: 10.1038/sj.bjp.0703393
- Scopus: eid_2-s2.0-0033920419
- PMID: 10882379
- WOS: WOS:000088067100002
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Article: Endothelial dysfunction in diabetes
Title | Endothelial dysfunction in diabetes |
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Authors | |
Keywords | Advanced glycation end products Aldose reductase Diabetes Endothelial dysfunction Endothelium-dependent vasodilation Endothelium-derived hyperpolarizing factor Nitric oxide Oxidative stress Protein kinase C |
Issue Date | 2000 |
Publisher | John Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1 |
Citation | British Journal Of Pharmacology, 2000, v. 130 n. 5, p. 963-974 How to Cite? |
Abstract | Endothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of different animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycaemia-induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non-enzymatic glycation and oxidative stress. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to differ according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction. |
Persistent Identifier | http://hdl.handle.net/10722/171236 |
ISSN | 2023 Impact Factor: 6.8 2023 SCImago Journal Rankings: 2.119 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | De Vriese, AS | en_US |
dc.contributor.author | Verbeuren, TJ | en_US |
dc.contributor.author | Van De Voorde, J | en_US |
dc.contributor.author | Lameire, NH | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:12:52Z | - |
dc.date.available | 2012-10-30T06:12:52Z | - |
dc.date.issued | 2000 | en_US |
dc.identifier.citation | British Journal Of Pharmacology, 2000, v. 130 n. 5, p. 963-974 | en_US |
dc.identifier.issn | 0007-1188 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171236 | - |
dc.description.abstract | Endothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of different animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycaemia-induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non-enzymatic glycation and oxidative stress. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to differ according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction. | en_US |
dc.language | eng | en_US |
dc.publisher | John Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1 | en_US |
dc.relation.ispartof | British Journal of Pharmacology | en_US |
dc.subject | Advanced glycation end products | - |
dc.subject | Aldose reductase | - |
dc.subject | Diabetes | - |
dc.subject | Endothelial dysfunction | - |
dc.subject | Endothelium-dependent vasodilation | - |
dc.subject | Endothelium-derived hyperpolarizing factor | - |
dc.subject | Nitric oxide | - |
dc.subject | Oxidative stress | - |
dc.subject | Protein kinase C | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Biological Factors - Physiology | en_US |
dc.subject.mesh | Diabetes Mellitus - Physiopathology | en_US |
dc.subject.mesh | Endothelins - Physiology | en_US |
dc.subject.mesh | Endothelium, Vascular - Physiopathology | en_US |
dc.subject.mesh | Glycosylation End Products, Advanced - Physiology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Nitric Oxide - Physiology | en_US |
dc.subject.mesh | Oxidative Stress | en_US |
dc.subject.mesh | Protein Kinase C - Physiology | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.subject.mesh | Vasodilation | en_US |
dc.title | Endothelial dysfunction in diabetes | 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.doi | 10.1038/sj.bjp.0703393 | - |
dc.identifier.pmid | 10882379 | - |
dc.identifier.scopus | eid_2-s2.0-0033920419 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0033920419&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 130 | en_US |
dc.identifier.issue | 5 | en_US |
dc.identifier.spage | 963 | en_US |
dc.identifier.epage | 974 | en_US |
dc.identifier.isi | WOS:000088067100002 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | De Vriese, AS=7006417891 | en_US |
dc.identifier.scopusauthorid | Verbeuren, TJ=7007006534 | en_US |
dc.identifier.scopusauthorid | Van De Voorde, J=7005936690 | en_US |
dc.identifier.scopusauthorid | Lameire, NH=35375565900 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0007-1188 | - |