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Article: Serotonin and the blood vessel wall

TitleSerotonin and the blood vessel wall
Authors
Issue Date1986
PublisherLippincott Williams & Wilkins, Ltd. The Journal's web site is located at http://www.jhypertension.com/
Citation
Journal Of Hypertension, 1986, v. 4 SUPPL. 1, p. S29-S35 How to Cite?
AbstractSerotonin has complex effects on the cardiovascular system. In the intact animal it may cause increases or decreases of blood pressure and in isolated blood vessels contraction or relaxation depending on the species and vascular bed studied, the route of administration and the dosage used. Contractions evoked by the monoamine are mediated mainly by S2-serotonergic receptors on vascular smooth muscle; in addition, serotonin may act indirectly by amplifying the response to norepinephrine and other agonists, by displacing norepinephrine from adrenergic nerve terminals or releasing constrictor substance(s) from the endothelium. Dilatation in response to serotonin is mediated by endothelial and prejunctional S1-serotonergic receptors which pharmacologically resemble 5-HT1-binding sites. In hypertension, constrictor responses to serotonin are augmented, while the vasodilator effects of the monoamine are decreased. The constrictor response to serotonin is increased more than those to other agonists, suggesting a functional rather than a structural adaptation of the hypertensive blood vessel wall. In hypertension the turnover of circulating platelets, the major source of peripheral serotonin, is accelerated and the mechanisms for the removal of the monoamine are impaired. The functional changes of the blood vessel wall and platelets could play a role in the maintenance of the increased peripheral vascular resistance in chronic hypertension, and they could be involved in the pathogenesis of complications of the hypertensive process. The concept that serotonin plays a role in chronic hypertension is further supported by the antihypertensive properties of the S2-serotonergic antagonist, ketanserin.
Persistent Identifierhttp://hdl.handle.net/10722/170835
ISSN
2015 Impact Factor: 5.062
2015 SCImago Journal Rankings: 2.193
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorLuscher, TFen_US
dc.date.accessioned2012-10-30T06:11:03Z-
dc.date.available2012-10-30T06:11:03Z-
dc.date.issued1986en_US
dc.identifier.citationJournal Of Hypertension, 1986, v. 4 SUPPL. 1, p. S29-S35en_US
dc.identifier.issn0263-6352en_US
dc.identifier.urihttp://hdl.handle.net/10722/170835-
dc.description.abstractSerotonin has complex effects on the cardiovascular system. In the intact animal it may cause increases or decreases of blood pressure and in isolated blood vessels contraction or relaxation depending on the species and vascular bed studied, the route of administration and the dosage used. Contractions evoked by the monoamine are mediated mainly by S2-serotonergic receptors on vascular smooth muscle; in addition, serotonin may act indirectly by amplifying the response to norepinephrine and other agonists, by displacing norepinephrine from adrenergic nerve terminals or releasing constrictor substance(s) from the endothelium. Dilatation in response to serotonin is mediated by endothelial and prejunctional S1-serotonergic receptors which pharmacologically resemble 5-HT1-binding sites. In hypertension, constrictor responses to serotonin are augmented, while the vasodilator effects of the monoamine are decreased. The constrictor response to serotonin is increased more than those to other agonists, suggesting a functional rather than a structural adaptation of the hypertensive blood vessel wall. In hypertension the turnover of circulating platelets, the major source of peripheral serotonin, is accelerated and the mechanisms for the removal of the monoamine are impaired. The functional changes of the blood vessel wall and platelets could play a role in the maintenance of the increased peripheral vascular resistance in chronic hypertension, and they could be involved in the pathogenesis of complications of the hypertensive process. The concept that serotonin plays a role in chronic hypertension is further supported by the antihypertensive properties of the S2-serotonergic antagonist, ketanserin.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins, Ltd. The Journal's web site is located at http://www.jhypertension.com/en_US
dc.relation.ispartofJournal of Hypertensionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Platelets - Metabolismen_US
dc.subject.meshHeart - Drug Effectsen_US
dc.subject.meshHypertension - Drug Therapy - Metabolismen_US
dc.subject.meshKetanserinen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPiperidines - Therapeutic Useen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshSerotonin - Metabolism - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleSerotonin and the blood vessel wallen_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.pmid2939211-
dc.identifier.scopuseid_2-s2.0-0023034537en_US
dc.identifier.volume4en_US
dc.identifier.issueSUPPL. 1en_US
dc.identifier.spageS29en_US
dc.identifier.epageS35en_US
dc.identifier.isiWOS:A1986C094200007-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridLuscher, TF=18935805600en_US

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