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- Publisher Website: 10.1006/jmcc.1998.0844
- Scopus: eid_2-s2.0-0033055559
- PMID: 10072716
- WOS: WOS:000078427700007
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Conference Paper: Endothelial dysfunction: From physiology to therapy
Title | Endothelial dysfunction: From physiology to therapy |
---|---|
Authors | |
Keywords | Angiotensin Bradykinin Endothelium-derived hyperpolarizing factor Kallikrein Kininogen Nitric oxide Prostacyclin Vascular smooth muscle |
Issue Date | 1999 |
Publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc |
Citation | Journal Of Molecular And Cellular Cardiology, 1999, v. 31 n. 1, p. 61-74 How to Cite? |
Abstract | The endothelium controls the tone of the underlying vascular smooth muscle mainly through the production of vasodilator mediators. In some cases, this function is hampered by the release of constrictor substances. The endothelial mediators are also involved in the regulation by the endothelium of vascular architecture and the blood cell-vascular wall interactions. The endothelium-derived factors comprise nitric oxide (NO), prostacyclin, and a still unknown endothelium-derived hyperpolarizing factor(s) (EDHF). In most vascular diseases, the vasodilator function of the endothelium is attenuated. In advanced atherosclerotic lesions, endothelium-dependent vasodilatation may even be abolished. Various degrees and forms of endothelial dysfunction exist, including (1) the impairment of G(αi) proteins, (2) less release of NO, prostacyclin and/or EDHF, (3) increased release of endoperoxides, (4) increased production of reactive oxygen species, (5) increased generation of endothelin-1, and (6) decreased sensitivity of the vascular smooth muscle to NO, prostacyclin and/or EDHF. The levels of bradykinin and angiotensin II within the vascular wall are controlled by angiotensin-conoerting enzyme (ACE). ACE degrades bradykinin and generates angiotensin II. Bradykinin stimulates endothelial cells to release vasodilators. The actions of the kinin are maintained despite endothelial dysfunction, except in very severe arterial lesions. Angiotensin II may be in part responsible for endothelial dysfunction because it induces resistance to the vasodilaor action of NO. Thus, impairment of the generation of angiotensin II blocks the direct and indirect vasoconstrictor effect of the peptide. By potentiating bradykinin, ACE inhibitors promote the release of relaxing vasodilator mediators to restore vasodilator function, and to prevent platelet aggregation as well as the recruitment of leukocytes to the vascular wall. |
Persistent Identifier | http://hdl.handle.net/10722/173536 |
ISSN | 2021 Impact Factor: 5.763 2020 SCImago Journal Rankings: 1.645 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Mombouli, JV | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:32:33Z | - |
dc.date.available | 2012-10-30T06:32:33Z | - |
dc.date.issued | 1999 | en_US |
dc.identifier.citation | Journal Of Molecular And Cellular Cardiology, 1999, v. 31 n. 1, p. 61-74 | en_US |
dc.identifier.issn | 0022-2828 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/173536 | - |
dc.description.abstract | The endothelium controls the tone of the underlying vascular smooth muscle mainly through the production of vasodilator mediators. In some cases, this function is hampered by the release of constrictor substances. The endothelial mediators are also involved in the regulation by the endothelium of vascular architecture and the blood cell-vascular wall interactions. The endothelium-derived factors comprise nitric oxide (NO), prostacyclin, and a still unknown endothelium-derived hyperpolarizing factor(s) (EDHF). In most vascular diseases, the vasodilator function of the endothelium is attenuated. In advanced atherosclerotic lesions, endothelium-dependent vasodilatation may even be abolished. Various degrees and forms of endothelial dysfunction exist, including (1) the impairment of G(αi) proteins, (2) less release of NO, prostacyclin and/or EDHF, (3) increased release of endoperoxides, (4) increased production of reactive oxygen species, (5) increased generation of endothelin-1, and (6) decreased sensitivity of the vascular smooth muscle to NO, prostacyclin and/or EDHF. The levels of bradykinin and angiotensin II within the vascular wall are controlled by angiotensin-conoerting enzyme (ACE). ACE degrades bradykinin and generates angiotensin II. Bradykinin stimulates endothelial cells to release vasodilators. The actions of the kinin are maintained despite endothelial dysfunction, except in very severe arterial lesions. Angiotensin II may be in part responsible for endothelial dysfunction because it induces resistance to the vasodilaor action of NO. Thus, impairment of the generation of angiotensin II blocks the direct and indirect vasoconstrictor effect of the peptide. By potentiating bradykinin, ACE inhibitors promote the release of relaxing vasodilator mediators to restore vasodilator function, and to prevent platelet aggregation as well as the recruitment of leukocytes to the vascular wall. | en_US |
dc.language | eng | en_US |
dc.publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc | en_US |
dc.relation.ispartof | Journal of Molecular and Cellular Cardiology | en_US |
dc.subject | Angiotensin | - |
dc.subject | Bradykinin | - |
dc.subject | Endothelium-derived hyperpolarizing factor | - |
dc.subject | Kallikrein | - |
dc.subject | Kininogen | - |
dc.subject | Nitric oxide | - |
dc.subject | Prostacyclin | - |
dc.subject | Vascular smooth muscle | - |
dc.subject.mesh | Aging | en_US |
dc.subject.mesh | Angiotensins - Pharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Arteriosclerosis - Metabolism | en_US |
dc.subject.mesh | Biological Factors - Physiology | en_US |
dc.subject.mesh | Bradykinin - Pharmacology | en_US |
dc.subject.mesh | Endothelins - Physiology | en_US |
dc.subject.mesh | Endothelium, Vascular - Physiology - Physiopathology | en_US |
dc.subject.mesh | Epoprostenol - Physiology | en_US |
dc.subject.mesh | Heart Failure - Metabolism - Therapy | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Hyperlipidemias - Metabolism | en_US |
dc.subject.mesh | Hypertension - Metabolism - Therapy | en_US |
dc.subject.mesh | Models, Biological | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular - Metabolism | en_US |
dc.subject.mesh | Nitric Oxide - Physiology | en_US |
dc.subject.mesh | Peptidyl-Dipeptidase A - Physiology | en_US |
dc.subject.mesh | Prostaglandins - Physiology | en_US |
dc.subject.mesh | Reactive Oxygen Species - Physiology | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.title | Endothelial dysfunction: From physiology to therapy | en_US |
dc.type | Conference_Paper | 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 | 10.1006/jmcc.1998.0844 | en_US |
dc.identifier.pmid | 10072716 | - |
dc.identifier.scopus | eid_2-s2.0-0033055559 | en_US |
dc.identifier.volume | 31 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 61 | en_US |
dc.identifier.epage | 74 | en_US |
dc.identifier.isi | WOS:000078427700007 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Mombouli, JV=7004285772 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0022-2828 | - |