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- Scopus: eid_2-s2.0-0025027155
- PMID: 2122922
- WOS: WOS:A1990EJ15600017
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Conference Paper: G-proteins and endothelial responses
Title | G-proteins and endothelial responses |
---|---|
Authors | |
Keywords | Atherosclerosis Endothelium-derived relaxing factor Guanine-nucleotide regulatory protein Hypercholesterolemia Pertussis toxin Vascular disease |
Issue Date | 1990 |
Publisher | S Karger AG. The Journal's web site is located at http://www.karger.com/JVR |
Citation | Blood Vessels, 1990, v. 27 n. 2-5, p. 218-229 How to Cite? |
Abstract | G-proteins are transducing proteins that couple a large number of membrane-bound receptors to a variety of intracellular effector systems. Pertussis toxin ADP-ribosylates certain G-proteins causing inhibition of their function. In porcine coronary arteries, pertussis toxin inhibited the endothelium-dependent relaxations evoked by alpha-2-adrenergic or serotonergic receptor stimulation, and by aggregating platelets or thrombin. Relaxations to nitric oxide and endothelium-dependent relaxations to bradykinin, adenosine diphosphate or A23187 were unaffected by the toxin. Therefore, certain endothelium-dependent relaxations are mediated by activation of a pertussis toxin-sensitive G-protein in the endothelial cells, most likely G(i)-protein. In porcine coronary arteries with regenerated endothelium (following in vivo denudation), the endothelium-dependent relaxations caused by the pertussis toxin-sensitive stimuli were reduced and were not further affected by pertussis toxin. Relaxations to be other stimuli were not altered by the regeneration process and were still not affected by the toxin. In regenerating endothelial cells there may be a selective impairment of the G-protein-dependent mechanism for releasing EDRF, which may predispose the blood vessel to vasospasm or the initiation of vascular disease. |
Persistent Identifier | http://hdl.handle.net/10722/173468 |
ISSN | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Flavahan, NA | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:32:13Z | - |
dc.date.available | 2012-10-30T06:32:13Z | - |
dc.date.issued | 1990 | en_US |
dc.identifier.citation | Blood Vessels, 1990, v. 27 n. 2-5, p. 218-229 | en_US |
dc.identifier.issn | 0303-6847 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/173468 | - |
dc.description.abstract | G-proteins are transducing proteins that couple a large number of membrane-bound receptors to a variety of intracellular effector systems. Pertussis toxin ADP-ribosylates certain G-proteins causing inhibition of their function. In porcine coronary arteries, pertussis toxin inhibited the endothelium-dependent relaxations evoked by alpha-2-adrenergic or serotonergic receptor stimulation, and by aggregating platelets or thrombin. Relaxations to nitric oxide and endothelium-dependent relaxations to bradykinin, adenosine diphosphate or A23187 were unaffected by the toxin. Therefore, certain endothelium-dependent relaxations are mediated by activation of a pertussis toxin-sensitive G-protein in the endothelial cells, most likely G(i)-protein. In porcine coronary arteries with regenerated endothelium (following in vivo denudation), the endothelium-dependent relaxations caused by the pertussis toxin-sensitive stimuli were reduced and were not further affected by pertussis toxin. Relaxations to be other stimuli were not altered by the regeneration process and were still not affected by the toxin. In regenerating endothelial cells there may be a selective impairment of the G-protein-dependent mechanism for releasing EDRF, which may predispose the blood vessel to vasospasm or the initiation of vascular disease. | en_US |
dc.language | eng | en_US |
dc.publisher | S Karger AG. The Journal's web site is located at http://www.karger.com/JVR | en_US |
dc.relation.ispartof | Blood Vessels | en_US |
dc.subject | Atherosclerosis | - |
dc.subject | Endothelium-derived relaxing factor | - |
dc.subject | Guanine-nucleotide regulatory protein | - |
dc.subject | Hypercholesterolemia | - |
dc.subject | Pertussis toxin | - |
dc.subject | Vascular disease | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Cardiovascular Diseases - Pathology | en_US |
dc.subject.mesh | Coronary Vessels - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Endothelium, Vascular - Drug Effects - Injuries - Metabolism | en_US |
dc.subject.mesh | Gtp-Binding Proteins - Physiology | en_US |
dc.subject.mesh | Nitric Oxide - Metabolism | en_US |
dc.subject.mesh | Pertussis Toxin | en_US |
dc.subject.mesh | Vasodilator Agents - Pharmacology | en_US |
dc.subject.mesh | Virulence Factors, Bordetella - Pharmacology | en_US |
dc.title | G-proteins and endothelial responses | 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 | 2122922 | - |
dc.identifier.scopus | eid_2-s2.0-0025027155 | en_US |
dc.identifier.volume | 27 | en_US |
dc.identifier.issue | 2-5 | en_US |
dc.identifier.spage | 218 | en_US |
dc.identifier.epage | 229 | en_US |
dc.identifier.isi | WOS:A1990EJ15600017 | - |
dc.publisher.place | Switzerland | en_US |
dc.identifier.scopusauthorid | Flavahan, NA=7006398882 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0303-6847 | - |