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Conference Paper: Vascular effects of serotonin and ischemia

TitleVascular effects of serotonin and ischemia
Authors
Issue Date1990
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1990, v. 16 SUPPL. 3, p. S15-S19 How to Cite?
AbstractCirculating 5-hydroxytryptamine originates in the gastrointestinal tract, where it overflows to the blood; part of that serotonin is taken up and stored by the platelets. When the latter aggregate, the released serotonin feeds back on the platelets to amplify the aggregation process; this amplification can be blocked with 5-HT2-serotonergic antagonists such as ketanserin and naftidrofuryl. Serotonin is taken up and destroyed by the endothelial cells; these cells also release endothelium-derived relaxing factor (EDRF) when exposed to the monoamine. The release of EDRF evoked by serotonin is not blocked by 5-HT2-serotonergic antagonists and involves a pertussis toxin-sensitive G-protein. When serotonin reaches vascular smooth muscle it usually causes it to contract; this, in most blood vessels, is prevented by 5-HT2-serotonergic antagonists. The contractions evoked by serotonin are reduced considerably in the presence of a normal endothelium. The same is true for contractions evoked by aggregating platelets, which release enough serotonin to activate receptors on both the endothelial cells (release of EDRF) and on vascular smooth muscle (contraction). Thus, 5-HT2-serotonergic antagonists favor vasodilatation not only because they brake the amplifying effect that serotonin exerts on further platelet aggregation, but also because, by blocking the direct activation of the vascular smooth muscle by platelet-released serotonin, they facilitate the occurrence of endothelium-dependent relaxations to the platelet products. These properties of 5-HT2-serotonergic antagonists help to explain a possible beneficial effect in the treatment of vascular disease, because atherosclerotic blood vessels exhibit a loss of the pertussis toxin-sensitive release of EDRF in response to serotonin, whereas the vasoconstrictor effect of the monoamine is augmented.
Persistent Identifierhttp://hdl.handle.net/10722/173483
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:17Z-
dc.date.available2012-10-30T06:32:17Z-
dc.date.issued1990en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1990, v. 16 SUPPL. 3, p. S15-S19en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173483-
dc.description.abstractCirculating 5-hydroxytryptamine originates in the gastrointestinal tract, where it overflows to the blood; part of that serotonin is taken up and stored by the platelets. When the latter aggregate, the released serotonin feeds back on the platelets to amplify the aggregation process; this amplification can be blocked with 5-HT2-serotonergic antagonists such as ketanserin and naftidrofuryl. Serotonin is taken up and destroyed by the endothelial cells; these cells also release endothelium-derived relaxing factor (EDRF) when exposed to the monoamine. The release of EDRF evoked by serotonin is not blocked by 5-HT2-serotonergic antagonists and involves a pertussis toxin-sensitive G-protein. When serotonin reaches vascular smooth muscle it usually causes it to contract; this, in most blood vessels, is prevented by 5-HT2-serotonergic antagonists. The contractions evoked by serotonin are reduced considerably in the presence of a normal endothelium. The same is true for contractions evoked by aggregating platelets, which release enough serotonin to activate receptors on both the endothelial cells (release of EDRF) and on vascular smooth muscle (contraction). Thus, 5-HT2-serotonergic antagonists favor vasodilatation not only because they brake the amplifying effect that serotonin exerts on further platelet aggregation, but also because, by blocking the direct activation of the vascular smooth muscle by platelet-released serotonin, they facilitate the occurrence of endothelium-dependent relaxations to the platelet products. These properties of 5-HT2-serotonergic antagonists help to explain a possible beneficial effect in the treatment of vascular disease, because atherosclerotic blood vessels exhibit a loss of the pertussis toxin-sensitive release of EDRF in response to serotonin, whereas the vasoconstrictor effect of the monoamine is augmented.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.meshAnimalsen_US
dc.subject.meshHumansen_US
dc.subject.meshIschemia - Drug Therapyen_US
dc.subject.meshSerotonin - Physiologyen_US
dc.subject.meshSerotonin Antagonists - Therapeutic Useen_US
dc.subject.meshVascular Diseases - Drug Therapyen_US
dc.subject.meshVasoconstrictionen_US
dc.subject.meshVasodilationen_US
dc.titleVascular effects of serotonin and ischemiaen_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.doi10.1097/00005344-199000163-00004-
dc.identifier.pmid1369711-
dc.identifier.scopuseid_2-s2.0-0025615923en_US
dc.identifier.volume16en_US
dc.identifier.issueSUPPL. 3en_US
dc.identifier.spageS15en_US
dc.identifier.epageS19en_US
dc.identifier.isiWOS:A1990EV31000004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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