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Article: Serotoninergic mechanisms in hypertension: Focus on the effects of ketanserin

TitleSerotoninergic mechanisms in hypertension: Focus on the effects of ketanserin
Authors
Issue Date1988
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1988, v. 11 n. 2, p. 111-133 How to Cite?
AbstractAggregating platelets release serotonin, which induces contraction of most vascular smooth muscle by activation of S 2-serotoninergic receptors. Serotonin released in the circulation may contribute to the increase in peripheral resistance of hypertension as the responsiveness of blood vessels from hypertensive animals and humans to the vasoconstrictor action of the monoamine is augmented. The data obtained with the new antihypertensive agent ketanserin may favor that interpretation. Ketanserin is a selective S 2-serotoninergic antagonist with additional α 1-adrenergic blocking properties. In humans, it has a terminal half-life of 12 to 25 hours and is eliminated predominantly by the liver. The hemodynamic profile of ketanserin is that of a vasodilator drug with actions on both resistance and capacitance vessels. On short-term intravenous administration, it lowers blood pressure in hypertensive patients with minimal reflex changes in cardiovascular function. When given orally long term to hypertensive patients, ketanserin causes a sustained reduction in arterial blood pressure, comparable to that obtained with either β-adrenergic blockers or diuretics. Several studies have shown a greater efficacy in older (>60 years of age) than in younger patients independent of starting pressure. Side effects mainly consist of dizziness, somnolence, and dry mouth, but they are usually not severe. The mechanism underlying the antihypertensive effect of ketanserin is unclear. It cannot be attributed to either S 2-serotoninergic or α 1-adrenergic blockade alone, but an interaction between the two effects appears to be required.
Persistent Identifierhttp://hdl.handle.net/10722/170888
ISSN
2015 Impact Factor: 6.294
2015 SCImago Journal Rankings: 3.702
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, Pen_US
dc.contributor.authorAmery, Aen_US
dc.contributor.authorBirkenhager, Wen_US
dc.contributor.authorBreckenridge, Aen_US
dc.contributor.authorBuhler, Fen_US
dc.contributor.authorDistler, Aen_US
dc.contributor.authorDormandy, Jen_US
dc.contributor.authorDoyle, Aen_US
dc.contributor.authorFrohlich, Een_US
dc.contributor.authorHansson, Len_US
dc.contributor.authorHedner, Ten_US
dc.contributor.authorHollenberg, Nen_US
dc.contributor.authorJensen, HEen_US
dc.contributor.authorLundJohansen, Pen_US
dc.contributor.authorMeyer, Pen_US
dc.contributor.authorOpie, Len_US
dc.contributor.authorRobertson, Ien_US
dc.contributor.authorSafar, Men_US
dc.contributor.authorSchalekamp, Men_US
dc.date.accessioned2012-10-30T06:11:18Z-
dc.date.available2012-10-30T06:11:18Z-
dc.date.issued1988en_US
dc.identifier.citationHypertension, 1988, v. 11 n. 2, p. 111-133en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170888-
dc.description.abstractAggregating platelets release serotonin, which induces contraction of most vascular smooth muscle by activation of S 2-serotoninergic receptors. Serotonin released in the circulation may contribute to the increase in peripheral resistance of hypertension as the responsiveness of blood vessels from hypertensive animals and humans to the vasoconstrictor action of the monoamine is augmented. The data obtained with the new antihypertensive agent ketanserin may favor that interpretation. Ketanserin is a selective S 2-serotoninergic antagonist with additional α 1-adrenergic blocking properties. In humans, it has a terminal half-life of 12 to 25 hours and is eliminated predominantly by the liver. The hemodynamic profile of ketanserin is that of a vasodilator drug with actions on both resistance and capacitance vessels. On short-term intravenous administration, it lowers blood pressure in hypertensive patients with minimal reflex changes in cardiovascular function. When given orally long term to hypertensive patients, ketanserin causes a sustained reduction in arterial blood pressure, comparable to that obtained with either β-adrenergic blockers or diuretics. Several studies have shown a greater efficacy in older (>60 years of age) than in younger patients independent of starting pressure. Side effects mainly consist of dizziness, somnolence, and dry mouth, but they are usually not severe. The mechanism underlying the antihypertensive effect of ketanserin is unclear. It cannot be attributed to either S 2-serotoninergic or α 1-adrenergic blockade alone, but an interaction between the two effects appears to be required.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_US
dc.relation.ispartofHypertensionen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension - Drug Therapy - Physiopathologyen_US
dc.subject.meshKetanserin - Pharmacokinetics - Therapeutic Useen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshReceptors, Serotonin - Drug Effectsen_US
dc.subject.meshSerotonin - Physiologyen_US
dc.titleSerotoninergic mechanisms in hypertension: Focus on the effects of ketanserinen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, P:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, P=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1161/01.HYP.11.2.111-
dc.identifier.pmid3277910-
dc.identifier.scopuseid_2-s2.0-0023841354en_US
dc.identifier.volume11en_US
dc.identifier.issue2en_US
dc.identifier.spage111en_US
dc.identifier.epage133en_US
dc.identifier.isiWOS:A1988M356400001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, P=7202304247en_US
dc.identifier.scopusauthoridAmery, A=35396947800en_US
dc.identifier.scopusauthoridBirkenhager, W=7103034367en_US
dc.identifier.scopusauthoridBreckenridge, A=7102002898en_US
dc.identifier.scopusauthoridBuhler, F=8838192300en_US
dc.identifier.scopusauthoridDistler, A=7102585048en_US
dc.identifier.scopusauthoridDormandy, J=7102485450en_US
dc.identifier.scopusauthoridDoyle, A=35397432900en_US
dc.identifier.scopusauthoridFrohlich, E=35392010300en_US
dc.identifier.scopusauthoridHansson, L=7403237277en_US
dc.identifier.scopusauthoridHedner, T=36038547500en_US
dc.identifier.scopusauthoridHollenberg, N=7101917199en_US
dc.identifier.scopusauthoridJensen, HE=16458584000en_US
dc.identifier.scopusauthoridLundJohansen, P=7006389141en_US
dc.identifier.scopusauthoridMeyer, P=7402019257en_US
dc.identifier.scopusauthoridOpie, L=36051372200en_US
dc.identifier.scopusauthoridRobertson, I=7202281692en_US
dc.identifier.scopusauthoridSafar, M=7202995824en_US
dc.identifier.scopusauthoridSchalekamp, M=18034871900en_US

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