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Article: Serotonin and vascular reactivity

TitleSerotonin and vascular reactivity
Authors
Issue Date1985
Citation
Pharmacological Research Communications, 1985, v. 17 n. 7, p. 585-608 How to Cite?
AbstractSerotonin causes contraction of the vascular smooth muscle cells in most blood vessels studied in vitro. This contraction is mainly due to activation of S2-serotonergic receptors. The monoamine can cause relaxation through activation of serotonergic receptors, different from the S2-serotonergic receptor and located on endothelial cells, or through an inhibitory effect on adrenergic neurotransmission. In certain blood vessels, the contractile effects can be markedly enhanced by hypoxia or moderate cooling. At low concentrations serotonin amplifies the vasoconstrictor responses to other vasoactive substances. Ultimately the effect of serotonin on vascular constriction is defined by the balance between these different actions. In the intact organism under normal conditions serotonin may play a modulatory role but exacerbation of the contractile effects because of hypersensitivity of the smooth muscle cells, local physical or humoral factors or loss of the relaxatory ability may lead to abnormal tissue responses. Thus, serotonin-induced vasoconstrictor responses may play a role in the etiology of vasospasm and peripheral vascular diseases, in particular at sites of endothelial lesions. Both the vasoconstrictor and the platelet aggregating effects of serotonin combined with its accelerated turnover may be important in the induction and maintenance of the augmented peripheral vascular resistance in arterial hypertension.
Persistent Identifierhttp://hdl.handle.net/10722/170801
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVan Nueten, JMen_US
dc.contributor.authorJanssens, WJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:54Z-
dc.date.available2012-10-30T06:10:54Z-
dc.date.issued1985en_US
dc.identifier.citationPharmacological Research Communications, 1985, v. 17 n. 7, p. 585-608en_US
dc.identifier.issn0031-6989en_US
dc.identifier.urihttp://hdl.handle.net/10722/170801-
dc.description.abstractSerotonin causes contraction of the vascular smooth muscle cells in most blood vessels studied in vitro. This contraction is mainly due to activation of S2-serotonergic receptors. The monoamine can cause relaxation through activation of serotonergic receptors, different from the S2-serotonergic receptor and located on endothelial cells, or through an inhibitory effect on adrenergic neurotransmission. In certain blood vessels, the contractile effects can be markedly enhanced by hypoxia or moderate cooling. At low concentrations serotonin amplifies the vasoconstrictor responses to other vasoactive substances. Ultimately the effect of serotonin on vascular constriction is defined by the balance between these different actions. In the intact organism under normal conditions serotonin may play a modulatory role but exacerbation of the contractile effects because of hypersensitivity of the smooth muscle cells, local physical or humoral factors or loss of the relaxatory ability may lead to abnormal tissue responses. Thus, serotonin-induced vasoconstrictor responses may play a role in the etiology of vasospasm and peripheral vascular diseases, in particular at sites of endothelial lesions. Both the vasoconstrictor and the platelet aggregating effects of serotonin combined with its accelerated turnover may be important in the induction and maintenance of the augmented peripheral vascular resistance in arterial hypertension.en_US
dc.languageengen_US
dc.relation.ispartofPharmacological Research Communicationsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshBlood Platelets - Metabolismen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCold Temperatureen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshKetanserinen_US
dc.subject.meshLidoflazine - Pharmacologyen_US
dc.subject.meshMethiothepin - Pharmacologyen_US
dc.subject.meshMethysergide - Pharmacologyen_US
dc.subject.meshMicrocirculationen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPiperidines - Pharmacologyen_US
dc.subject.meshReceptors, Serotonin - Metabolismen_US
dc.subject.meshRegional Blood Flowen_US
dc.subject.meshSerotonin - Physiologyen_US
dc.subject.meshSerotonin Antagonists - Pharmacologyen_US
dc.subject.meshVasoconstrictionen_US
dc.subject.meshVasodilationen_US
dc.titleSerotonin and vascular reactivityen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0031-6989(85)90067-0-
dc.identifier.pmid2931729-
dc.identifier.scopuseid_2-s2.0-0022403786en_US
dc.identifier.volume17en_US
dc.identifier.issue7en_US
dc.identifier.spage585en_US
dc.identifier.epage608en_US
dc.identifier.isiWOS:A1985APD0800001-
dc.identifier.scopusauthoridVan Nueten, JM=7005700327en_US
dc.identifier.scopusauthoridJanssens, WJ=7006876881en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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