File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Platelet-derived serotonin, the endothelium, and cardiovascular disease

TitlePlatelet-derived serotonin, the endothelium, and cardiovascular disease
Authors
Issue Date1991
PublisherLippincott 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?
AbstractThe 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 Identifierhttp://hdl.handle.net/10722/173491
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:20Z-
dc.date.available2012-10-30T06:32:20Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1991, v. 17 SUPPL. 5, p. S6-S12en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173491-
dc.description.abstractThe 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.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshBlood Platelets - Metabolismen_US
dc.subject.meshCardiovascular Diseases - Metabolism - Physiopathologyen_US
dc.subject.meshEndothelins - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Secretionen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshSerotonin - Metabolismen_US
dc.titlePlatelet-derived serotonin, the endothelium, and cardiovascular diseaseen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-199100175-00002en_US
dc.identifier.pmid1717775-
dc.identifier.scopuseid_2-s2.0-0025943452en_US
dc.identifier.volume17en_US
dc.identifier.issueSUPPL. 5en_US
dc.identifier.spageS6en_US
dc.identifier.epageS12en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats