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Article: Serotonin, hypertension and vascular disease

TitleSerotonin, hypertension and vascular disease
Authors
Issue Date1991
Citation
Netherlands Journal Of Medicine, 1991, v. 38 n. 1, p. 35-42 How to Cite?
AbstractCirculating 5-hydroxytryptamine (5HT, serotonin) originates in the gastrointestinal tract where it overflows to the blood; part of that serotonin is taken up and stored by the platelets. When the platelets aggregate, the released serotonin feeds back on the platelets to amplify the aggregation process; this amplification can be blocked with 5HT2-serotonergic antagonists. Serotonin is taken up and destroyed by the endothelial cells; these cells also release endothelium-derived relaxing factor (EDRF) when exposed to the monoamine. The release of EDRF evoked by serotonin is not prevented by 5HT2-serotonergic antagonists, and involves a pertussis toxin-sensitive G-protein. When serotonin reaches vascular smooth muscle it usually causes it to contract; this, in most blood vessels, is prevented by 5HT2-serotonergic antagonists. The contractions evoked by serotonin are reduced considerably in the presence of a normal endothelium. The same is true for contractions evoked by aggregating platelets, which release enough serotonin to activate receptors on both the endothelial cells (release of EDRF) and on vascular smooth muscle (contraction). Thus, 5HT2-serotonergic antagonists favour vasodilatation not only because they brake the amplifying effect that serotonin exerts on further platelet aggregation, but also because, by blocking the direct activation of the vascular smooth muscle by platelet-released serotonin, they facilitate the occurrence of endothelium-dependent relaxations to the platelet-products. In addition, these compounds may prevent the stimulatory effect of serotonin on the proliferation of vascular smooth muscle. These properties of 5HT2-serotonergic antagonists help to explain a possible beneficial effect in the treatment of hypertension and vascular disease, since hypertensive and atherosclerotic blood vessels exhibit a loss of endothelium-dependent relaxations, while the vasoconstrictor effect of the monoamine is augmented.
Persistent Identifierhttp://hdl.handle.net/10722/171032
ISSN
2015 Impact Factor: 1.489
2015 SCImago Journal Rankings: 0.725
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:54Z-
dc.date.available2012-10-30T06:11:54Z-
dc.date.issued1991en_US
dc.identifier.citationNetherlands Journal Of Medicine, 1991, v. 38 n. 1, p. 35-42en_US
dc.identifier.issn0300-2977en_US
dc.identifier.urihttp://hdl.handle.net/10722/171032-
dc.description.abstractCirculating 5-hydroxytryptamine (5HT, serotonin) originates in the gastrointestinal tract where it overflows to the blood; part of that serotonin is taken up and stored by the platelets. When the platelets aggregate, the released serotonin feeds back on the platelets to amplify the aggregation process; this amplification can be blocked with 5HT2-serotonergic antagonists. Serotonin is taken up and destroyed by the endothelial cells; these cells also release endothelium-derived relaxing factor (EDRF) when exposed to the monoamine. The release of EDRF evoked by serotonin is not prevented by 5HT2-serotonergic antagonists, and involves a pertussis toxin-sensitive G-protein. When serotonin reaches vascular smooth muscle it usually causes it to contract; this, in most blood vessels, is prevented by 5HT2-serotonergic antagonists. The contractions evoked by serotonin are reduced considerably in the presence of a normal endothelium. The same is true for contractions evoked by aggregating platelets, which release enough serotonin to activate receptors on both the endothelial cells (release of EDRF) and on vascular smooth muscle (contraction). Thus, 5HT2-serotonergic antagonists favour vasodilatation not only because they brake the amplifying effect that serotonin exerts on further platelet aggregation, but also because, by blocking the direct activation of the vascular smooth muscle by platelet-released serotonin, they facilitate the occurrence of endothelium-dependent relaxations to the platelet-products. In addition, these compounds may prevent the stimulatory effect of serotonin on the proliferation of vascular smooth muscle. These properties of 5HT2-serotonergic antagonists help to explain a possible beneficial effect in the treatment of hypertension and vascular disease, since hypertensive and atherosclerotic blood vessels exhibit a loss of endothelium-dependent relaxations, while the vasoconstrictor effect of the monoamine is augmented.en_US
dc.languageengen_US
dc.relation.ispartofNetherlands Journal of Medicineen_US
dc.subject.meshBlood Platelets - Physiologyen_US
dc.subject.meshEndothelins - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension - Blood - Prevention & Controlen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshPlatelet Aggregation - Physiologyen_US
dc.subject.meshSerotonin - Blooden_US
dc.subject.meshSerotonin Antagonists - Administration & Dosage - Metabolismen_US
dc.subject.meshVascular Diseases - Blood - Prevention & Controlen_US
dc.subject.meshVasoconstriction - Drug Effects - Physiologyen_US
dc.titleSerotonin, hypertension and vascular diseaseen_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.pmid2030808-
dc.identifier.scopuseid_2-s2.0-0026097787en_US
dc.identifier.volume38en_US
dc.identifier.issue1en_US
dc.identifier.spage35en_US
dc.identifier.epage42en_US
dc.identifier.isiWOS:A1991FF19000008-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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