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- Publisher Website: 10.1016/0031-6989(85)90067-0
- Scopus: eid_2-s2.0-0022403786
- PMID: 2931729
- WOS: WOS:A1985APD0800001
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Article: Serotonin and vascular reactivity
Title | Serotonin and vascular reactivity |
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Authors | |
Issue Date | 1985 |
Citation | Pharmacological Research Communications, 1985, v. 17 n. 7, p. 585-608 How to Cite? |
Abstract | Serotonin 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 Identifier | http://hdl.handle.net/10722/170801 |
ISSN | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Van Nueten, JM | en_US |
dc.contributor.author | Janssens, WJ | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:10:54Z | - |
dc.date.available | 2012-10-30T06:10:54Z | - |
dc.date.issued | 1985 | en_US |
dc.identifier.citation | Pharmacological Research Communications, 1985, v. 17 n. 7, p. 585-608 | en_US |
dc.identifier.issn | 0031-6989 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170801 | - |
dc.description.abstract | Serotonin 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.language | eng | en_US |
dc.relation.ispartof | Pharmacological Research Communications | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Anoxia - Physiopathology | en_US |
dc.subject.mesh | Blood Platelets - Metabolism | en_US |
dc.subject.mesh | Calcium - Metabolism | en_US |
dc.subject.mesh | Cold Temperature | en_US |
dc.subject.mesh | Electric Stimulation | en_US |
dc.subject.mesh | Ketanserin | en_US |
dc.subject.mesh | Lidoflazine - Pharmacology | en_US |
dc.subject.mesh | Methiothepin - Pharmacology | en_US |
dc.subject.mesh | Methysergide - Pharmacology | en_US |
dc.subject.mesh | Microcirculation | en_US |
dc.subject.mesh | Models, Biological | en_US |
dc.subject.mesh | Muscle Contraction - Drug Effects | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular - Drug Effects | en_US |
dc.subject.mesh | Piperidines - Pharmacology | en_US |
dc.subject.mesh | Receptors, Serotonin - Metabolism | en_US |
dc.subject.mesh | Regional Blood Flow | en_US |
dc.subject.mesh | Serotonin - Physiology | en_US |
dc.subject.mesh | Serotonin Antagonists - Pharmacology | en_US |
dc.subject.mesh | Vasoconstriction | en_US |
dc.subject.mesh | Vasodilation | en_US |
dc.title | Serotonin and vascular reactivity | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/0031-6989(85)90067-0 | - |
dc.identifier.pmid | 2931729 | - |
dc.identifier.scopus | eid_2-s2.0-0022403786 | en_US |
dc.identifier.volume | 17 | en_US |
dc.identifier.issue | 7 | en_US |
dc.identifier.spage | 585 | en_US |
dc.identifier.epage | 608 | en_US |
dc.identifier.isi | WOS:A1985APD0800001 | - |
dc.identifier.scopusauthorid | Van Nueten, JM=7005700327 | en_US |
dc.identifier.scopusauthorid | Janssens, WJ=7006876881 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0031-6989 | - |