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- Scopus: eid_2-s2.0-0030469192
- PMID: 9120689
- WOS: WOS:A1996WE73800012
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Conference Paper: Endothelial dysfunction in hypertension
Title | Endothelial dysfunction in hypertension |
---|---|
Authors | |
Keywords | Endoperoxides Endothelium-dependent contracting factor Endothelium-derived hyperpolarizing factor Nitric oxide Thromboxane A2 |
Issue Date | 1996 |
Citation | Journal Of Hypertension, Supplement, 1996, v. 14 n. 5, p. S83-S93 How to Cite? |
Abstract | Purpose. To summarize how abnormal release of relaxing and contracting factors from endothelial cells contribute to the vascular abnormalities in hypertension. Endothelium-derived factors. The endothelium controls the tone of the underlying vascular smooth muscle by releasing relaxing and contracting factors. The former include prostacyclin, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), and the latter endoperoxides, thromboxane A2, superoxide anions and endothelin. Hypertension In most types of hypertension, endothelium-dependent relaxations are curtailed, because of a reduced production and/or action of endothelium-derived NO and EDHF. In essential hypertension, endothelium-dependent relaxations are reduced also because of the endothelium-dependent production of vasoconstrictor prostanoids (endoperoxides and, in some cases, thromboxane A2). Cause or consequence. The endothelial dysfunction observed in hypertensive blood vessels is likely to be a consequence rather than a cause of the disease process. Therapeutic implications. Enhanced release of endothelium-derived relaxing factors (NO and EDHF) help to explain the therapeutic effects of inhibitors of converting enzyme. |
Persistent Identifier | http://hdl.handle.net/10722/173528 |
ISSN | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:32:31Z | - |
dc.date.available | 2012-10-30T06:32:31Z | - |
dc.date.issued | 1996 | en_US |
dc.identifier.citation | Journal Of Hypertension, Supplement, 1996, v. 14 n. 5, p. S83-S93 | en_US |
dc.identifier.issn | 0952-1178 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/173528 | - |
dc.description.abstract | Purpose. To summarize how abnormal release of relaxing and contracting factors from endothelial cells contribute to the vascular abnormalities in hypertension. Endothelium-derived factors. The endothelium controls the tone of the underlying vascular smooth muscle by releasing relaxing and contracting factors. The former include prostacyclin, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), and the latter endoperoxides, thromboxane A2, superoxide anions and endothelin. Hypertension In most types of hypertension, endothelium-dependent relaxations are curtailed, because of a reduced production and/or action of endothelium-derived NO and EDHF. In essential hypertension, endothelium-dependent relaxations are reduced also because of the endothelium-dependent production of vasoconstrictor prostanoids (endoperoxides and, in some cases, thromboxane A2). Cause or consequence. The endothelial dysfunction observed in hypertensive blood vessels is likely to be a consequence rather than a cause of the disease process. Therapeutic implications. Enhanced release of endothelium-derived relaxing factors (NO and EDHF) help to explain the therapeutic effects of inhibitors of converting enzyme. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Journal of Hypertension, Supplement | en_US |
dc.subject | Endoperoxides | - |
dc.subject | Endothelium-dependent contracting factor | - |
dc.subject | Endothelium-derived hyperpolarizing factor | - |
dc.subject | Nitric oxide | - |
dc.subject | Thromboxane A2 | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Endothelium, Vascular - Physiopathology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Hypertension - Drug Therapy - Physiopathology | en_US |
dc.subject.mesh | Vasoconstriction - Physiology | en_US |
dc.subject.mesh | Vasodilation - Physiology | en_US |
dc.title | Endothelial dysfunction in hypertension | 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.pmid | 9120689 | - |
dc.identifier.scopus | eid_2-s2.0-0030469192 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0030469192&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 14 | en_US |
dc.identifier.issue | 5 | en_US |
dc.identifier.spage | S83 | en_US |
dc.identifier.epage | S93 | en_US |
dc.identifier.isi | WOS:A1996WE73800012 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0952-1178 | - |