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Article: Cardiovascular effects of serotonin

TitleCardiovascular effects of serotonin
Authors
Issue Date1987
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1987, v. 10 SUPPL. 3, p. S8-S11 How to Cite?
AbstractThe major target for circulating serotonin (released from aggregating platelets) appears to be the blood vessel wall (although little evidence is available), suggesting a role for the monoamine in controlling cardiac function. In cerebral blood vessels, serotonergic neurons are present, implying a potential serotonergic neurogenic control. Serotonin causes contraction of most large arteries and veins; it also causes contraction of venules. This is due mainly to direct activation of vascular smooth muscle, although amplification of the response to other endogenous vasoconstrictors (e.g., angiotensin II and norepinephrine) as well as facilitated release of norepinephrine may contribute. In peripheral blood vessels, the receptors mediating the contractions evoked by serotonin belong mainly to the 5-HT2-serotonergic subtype; in the coronary and cerebral arteries, this need not be the case. Vasodilator responses to serotonin are seen mainly at the arteriolar level, but they can also be observed in larger blood vessels. They can be caused by the release of other endogenous vasodilators (e.g., vasoactive intestinal polypeptide), direct relaxation of vascular smooth muscle, inhibition of adrenergic neurotransmission, or production of endothelium-derived relaxing factor(s). The dilator responses to serotonin are mediated by receptors with characteristics similar to 5-HT1-serotonergic binding sites. Aggregating platelets release enough serotonin to evoke both constrictor and dilator responses. The absence of endothelium may change the primary response to aggregating platelets from relaxation to contraction. The responsiveness of the blood vessel wall to serotonin can be augmented acutely by local hypoxia or by cooling. It is exaggerated in blood vessels taken from hypertensive or atherosclerotic animals. In hypertensive blood vessels, vasoconstrictor responses to serotonin may be augmented by the release of endothelium-derived contracting factor(s). Vasoconstrictor responses to serotonin may play a role in the etiology of vasospasm or in the maintenance of the augmented peripheral resistance in certain cases of arterial hypertension.
Persistent Identifierhttp://hdl.handle.net/10722/170849
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.accessioned2012-10-30T06:11:06Z-
dc.date.available2012-10-30T06:11:06Z-
dc.date.issued1987en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1987, v. 10 SUPPL. 3, p. S8-S11en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170849-
dc.description.abstractThe major target for circulating serotonin (released from aggregating platelets) appears to be the blood vessel wall (although little evidence is available), suggesting a role for the monoamine in controlling cardiac function. In cerebral blood vessels, serotonergic neurons are present, implying a potential serotonergic neurogenic control. Serotonin causes contraction of most large arteries and veins; it also causes contraction of venules. This is due mainly to direct activation of vascular smooth muscle, although amplification of the response to other endogenous vasoconstrictors (e.g., angiotensin II and norepinephrine) as well as facilitated release of norepinephrine may contribute. In peripheral blood vessels, the receptors mediating the contractions evoked by serotonin belong mainly to the 5-HT2-serotonergic subtype; in the coronary and cerebral arteries, this need not be the case. Vasodilator responses to serotonin are seen mainly at the arteriolar level, but they can also be observed in larger blood vessels. They can be caused by the release of other endogenous vasodilators (e.g., vasoactive intestinal polypeptide), direct relaxation of vascular smooth muscle, inhibition of adrenergic neurotransmission, or production of endothelium-derived relaxing factor(s). The dilator responses to serotonin are mediated by receptors with characteristics similar to 5-HT1-serotonergic binding sites. Aggregating platelets release enough serotonin to evoke both constrictor and dilator responses. The absence of endothelium may change the primary response to aggregating platelets from relaxation to contraction. The responsiveness of the blood vessel wall to serotonin can be augmented acutely by local hypoxia or by cooling. It is exaggerated in blood vessels taken from hypertensive or atherosclerotic animals. In hypertensive blood vessels, vasoconstrictor responses to serotonin may be augmented by the release of endothelium-derived contracting factor(s). Vasoconstrictor responses to serotonin may play a role in the etiology of vasospasm or in the maintenance of the augmented peripheral resistance in certain cases of arterial hypertension.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.meshCardiovascular System - Drug Effectsen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.titleCardiovascular effects of serotoninen_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.pmid2446079-
dc.identifier.scopuseid_2-s2.0-0023203208en_US
dc.identifier.volume10en_US
dc.identifier.issueSUPPL. 3en_US
dc.identifier.spageS8en_US
dc.identifier.epageS11en_US
dc.identifier.isiWOS:A1987K114200004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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