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Article: Serotonin and the vascular system: Role in health and disease, and implications for therapy

TitleSerotonin and the vascular system: Role in health and disease, and implications for therapy
Authors
Issue Date1986
PublisherAdis International Ltd. The Journal's web site is located at http://drugs.adisonline.com/
Citation
Drugs, 1986, v. 31 n. 2, p. 149-163 How to Cite?
AbstractSerotonin released from aggregating platelets can reach sufficient concentrations to affect local vascular function in a number of ways. The monoamine can cause contraction of blood vessels by its direct action on smooth muscle or by potentiating the effect of other vasoconstrictor agents. It can also induce vasodilatation by a direct relaxing effect on smooth muscle, by inhibition of adrenergic nerves, and by release of an uncharacterised relaxing factor from endothelial cells. One of its most likely physiological roles is to aid in haemostasis by promoting platelet aggregation and by causing local vasoconstriction at sites of injury. It probably has a role in some forms of vascular pathology as well: it may contribute to vasospasms of cerebral, coronary, and digital arteries, particularly if there is endothelial dysfunction or damage. Much evidence has implicated serotonin (5-hydroxytryptamine) in the pathogenesis of migraine. Serotonergic agonists, such as ergotamine, and antagonists, such as methysergide and pizotifen, are both used in therapy of migraine. Promising but conflicting early results have not yet defined a place for serotonergic antagonists in other vasospastic disorders. The antihypertensive efficacy of one serotonergic antagonist, ketanserin, raises questions about the possible involvement of serotonin in either the initiation or the maintenance of the elevated peripheral vascular resistance in several forms of hypertension, including essential hypertension.
Persistent Identifierhttp://hdl.handle.net/10722/170821
ISSN
2015 Impact Factor: 4.883
2015 SCImago Journal Rankings: 1.601
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHouston, DSen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:00Z-
dc.date.available2012-10-30T06:11:00Z-
dc.date.issued1986en_US
dc.identifier.citationDrugs, 1986, v. 31 n. 2, p. 149-163en_US
dc.identifier.issn0012-6667en_US
dc.identifier.urihttp://hdl.handle.net/10722/170821-
dc.description.abstractSerotonin released from aggregating platelets can reach sufficient concentrations to affect local vascular function in a number of ways. The monoamine can cause contraction of blood vessels by its direct action on smooth muscle or by potentiating the effect of other vasoconstrictor agents. It can also induce vasodilatation by a direct relaxing effect on smooth muscle, by inhibition of adrenergic nerves, and by release of an uncharacterised relaxing factor from endothelial cells. One of its most likely physiological roles is to aid in haemostasis by promoting platelet aggregation and by causing local vasoconstriction at sites of injury. It probably has a role in some forms of vascular pathology as well: it may contribute to vasospasms of cerebral, coronary, and digital arteries, particularly if there is endothelial dysfunction or damage. Much evidence has implicated serotonin (5-hydroxytryptamine) in the pathogenesis of migraine. Serotonergic agonists, such as ergotamine, and antagonists, such as methysergide and pizotifen, are both used in therapy of migraine. Promising but conflicting early results have not yet defined a place for serotonergic antagonists in other vasospastic disorders. The antihypertensive efficacy of one serotonergic antagonist, ketanserin, raises questions about the possible involvement of serotonin in either the initiation or the maintenance of the elevated peripheral vascular resistance in several forms of hypertension, including essential hypertension.en_US
dc.languageengen_US
dc.publisherAdis International Ltd. The Journal's web site is located at http://drugs.adisonline.com/en_US
dc.relation.ispartofDrugsen_US
dc.subject.meshBlood Platelets - Drug Effectsen_US
dc.subject.meshCardiovascular Diseases - Drug Therapy - Physiopathologyen_US
dc.subject.meshCardiovascular Physiological Phenomenaen_US
dc.subject.meshEndothelium - Cytologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHemostasisen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshHypertension, Pulmonary - Physiopathologyen_US
dc.subject.meshMalignant Carcinoid Syndrome - Physiopathologyen_US
dc.subject.meshMigraine Disorders - Physiopathologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNerve Endings - Drug Effectsen_US
dc.subject.meshPre-Eclampsia - Physiopathologyen_US
dc.subject.meshPregnancyen_US
dc.subject.meshReceptors, Serotonin - Drug Effectsen_US
dc.subject.meshRegional Blood Flowen_US
dc.subject.meshSerotonin - Pharmacology - Physiologyen_US
dc.subject.meshVascular Diseases - Physiopathologyen_US
dc.titleSerotonin and the vascular system: Role in health and disease, and implications for therapyen_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.doi10.2165/00003495-198631020-00004-
dc.identifier.pmid3512233-
dc.identifier.scopuseid_2-s2.0-0022629332en_US
dc.identifier.volume31en_US
dc.identifier.issue2en_US
dc.identifier.spage149en_US
dc.identifier.epage163en_US
dc.identifier.isiWOS:A1986AYZ0600004-
dc.publisher.placeNew Zealanden_US
dc.identifier.scopusauthoridHouston, DS=35966326400en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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