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- Publisher Website: 10.1097/00005344-199100175-00002
- Scopus: eid_2-s2.0-0025943452
- PMID: 1717775
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Conference Paper: Platelet-derived serotonin, the endothelium, and cardiovascular disease
Title | Platelet-derived serotonin, the endothelium, and cardiovascular disease |
---|---|
Authors | |
Keywords | Endothelium-derived relaxing factor Serotonin Vascular smooth muscle |
Issue Date | 1991 |
Publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ |
Citation | Journal Of Cardiovascular Pharmacology, 1991, v. 17 SUPPL. 5, p. S6-S12 How to Cite? |
Abstract | The endothelial cells can release both relaxing and contracting substances. The former include prostacyclin and endothelium-derived relaxing factor (EDRF, which most likely is nitric oxide, or a nitrosoderivative releasing nitric oxide, derived from L-arginine). Candidates as endothelium-derived contracting factors (EDCF) include superoxide anions thromboxane A2 and the peptide endothelin. Endothelium-derived relaxing factor causes relaxation of vascular smooth muscle by activation of the soluble form of guanylate cyclase which leads to an accumulation of cyclic GMP; it also reduces platelet adhesion and aggregation. The latter effect is synergistic with the inhibition evoked by prostacyclin. The release of EDRF and prostacyclin plays a key role in the protective role of the endothelium against vasospasm and the unwanted coagulation of blood. Indeed, thrombin and aggregating platelets are potent stimuli for the release of EDRF. The platelet-products responsible are the adenine nucleotides, ADP and ATP, which activate P(2y)-purinergic receptors on the endothelial cells and 5-hydroxytryptamine (serotonin) that stimulates 5-HT1-like serotonergic receptors. The response to serotonin, but not that to the adenine nucleotides, is mediated by a pertussis toxin-sensitive mechanism. When endothelial cells regenerate, or are cultured, they selectively lose the pertussis toxin-sensitive mechanism of release, which results in a marked decrease in sensitivity to exogenous and platelet-released serotonin. As a consequence, the endothelial cells exhibit a considerably reduced response to aggregating platelets. This phenomenon, which can be exacerbated by hypercholesterolemia, favors ongoing platelet aggregation and vasospasm, and constitutes a first step toward atherosclerosis. |
Persistent Identifier | http://hdl.handle.net/10722/173491 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.610 |
DC Field | Value | Language |
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dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:32:20Z | - |
dc.date.available | 2012-10-30T06:32:20Z | - |
dc.date.issued | 1991 | en_US |
dc.identifier.citation | Journal Of Cardiovascular Pharmacology, 1991, v. 17 SUPPL. 5, p. S6-S12 | en_US |
dc.identifier.issn | 0160-2446 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/173491 | - |
dc.description.abstract | The endothelial cells can release both relaxing and contracting substances. The former include prostacyclin and endothelium-derived relaxing factor (EDRF, which most likely is nitric oxide, or a nitrosoderivative releasing nitric oxide, derived from L-arginine). Candidates as endothelium-derived contracting factors (EDCF) include superoxide anions thromboxane A2 and the peptide endothelin. Endothelium-derived relaxing factor causes relaxation of vascular smooth muscle by activation of the soluble form of guanylate cyclase which leads to an accumulation of cyclic GMP; it also reduces platelet adhesion and aggregation. The latter effect is synergistic with the inhibition evoked by prostacyclin. The release of EDRF and prostacyclin plays a key role in the protective role of the endothelium against vasospasm and the unwanted coagulation of blood. Indeed, thrombin and aggregating platelets are potent stimuli for the release of EDRF. The platelet-products responsible are the adenine nucleotides, ADP and ATP, which activate P(2y)-purinergic receptors on the endothelial cells and 5-hydroxytryptamine (serotonin) that stimulates 5-HT1-like serotonergic receptors. The response to serotonin, but not that to the adenine nucleotides, is mediated by a pertussis toxin-sensitive mechanism. When endothelial cells regenerate, or are cultured, they selectively lose the pertussis toxin-sensitive mechanism of release, which results in a marked decrease in sensitivity to exogenous and platelet-released serotonin. As a consequence, the endothelial cells exhibit a considerably reduced response to aggregating platelets. This phenomenon, which can be exacerbated by hypercholesterolemia, favors ongoing platelet aggregation and vasospasm, and constitutes a first step toward atherosclerosis. | en_US |
dc.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ | en_US |
dc.relation.ispartof | Journal of Cardiovascular Pharmacology | en_US |
dc.subject | Endothelium-derived relaxing factor | - |
dc.subject | Serotonin | - |
dc.subject | Vascular smooth muscle | - |
dc.subject.mesh | Blood Platelets - Metabolism | en_US |
dc.subject.mesh | Cardiovascular Diseases - Metabolism - Physiopathology | en_US |
dc.subject.mesh | Endothelins - Physiology | en_US |
dc.subject.mesh | Endothelium, Vascular - Secretion | en_US |
dc.subject.mesh | Nitric Oxide - Physiology | en_US |
dc.subject.mesh | Serotonin - Metabolism | en_US |
dc.title | Platelet-derived serotonin, the endothelium, and cardiovascular disease | 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 | 10.1097/00005344-199100175-00002 | en_US |
dc.identifier.pmid | 1717775 | - |
dc.identifier.scopus | eid_2-s2.0-0025943452 | en_US |
dc.identifier.volume | 17 | en_US |
dc.identifier.issue | SUPPL. 5 | en_US |
dc.identifier.spage | S6 | en_US |
dc.identifier.epage | S12 | en_US |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0160-2446 | - |