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Article: Calcium antagonism and vascular smooth muscle

TitleCalcium antagonism and vascular smooth muscle
Authors
Issue Date1988
PublisherWiley-Blackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journal.asp?ref=0077-8923&site=1
Citation
Annals Of The New York Academy Of Sciences, 1988, v. 522, p. 234-247 How to Cite?
AbstractVasoconstriction results from an exaggerated increase of intracellular Ca2+ concentration which initiates the contractile process within the vascular smooth muscle. The dependency of these cells on extracellular Ca2+ to trigger the contractile process when exposed to naturally occurring vasoactive substances such as those released from aggregating blood platelets varies in different vascular areas. This is one of the factors that determine the different sensitivity to the inhibitory effect of various calcium antagonists. A blood vessel can be more reactive to some calcium antagonists than to others, depending on the vascular area. Experiments on isolated cerebral arteries suggest that inhibition of cerebral vasoconstriction is observed with substances such as flunarizine under conditions of vascular hyperresponsiveness generated by acute or chronic pathological conditions or triggered by interaction between vasoactive substances. In this regard marked differences exist between the individual calcium antagonists. Those that are selective for slow Ca2+ channels will inhibit myocardial contractile force and decrease vascular myogenic activity (e.g., at the arteriolar level). Such inhibitory activity is not observed with flunarizine, which affects Ca2+ entry rather selectively, when calcium overload is imposed upon the vasculature, in particular at cerebrovascular sites. This suggests a potential use of this compound in a number of neurological disorders related to cerebral ischemia.
Persistent Identifierhttp://hdl.handle.net/10722/170881
ISSN
2015 Impact Factor: 4.518
2015 SCImago Journal Rankings: 2.389
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVan Nueten, JMen_US
dc.contributor.authorJanssens, WJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:15Z-
dc.date.available2012-10-30T06:11:15Z-
dc.date.issued1988en_US
dc.identifier.citationAnnals Of The New York Academy Of Sciences, 1988, v. 522, p. 234-247en_US
dc.identifier.issn0077-8923en_US
dc.identifier.urihttp://hdl.handle.net/10722/170881-
dc.description.abstractVasoconstriction results from an exaggerated increase of intracellular Ca2+ concentration which initiates the contractile process within the vascular smooth muscle. The dependency of these cells on extracellular Ca2+ to trigger the contractile process when exposed to naturally occurring vasoactive substances such as those released from aggregating blood platelets varies in different vascular areas. This is one of the factors that determine the different sensitivity to the inhibitory effect of various calcium antagonists. A blood vessel can be more reactive to some calcium antagonists than to others, depending on the vascular area. Experiments on isolated cerebral arteries suggest that inhibition of cerebral vasoconstriction is observed with substances such as flunarizine under conditions of vascular hyperresponsiveness generated by acute or chronic pathological conditions or triggered by interaction between vasoactive substances. In this regard marked differences exist between the individual calcium antagonists. Those that are selective for slow Ca2+ channels will inhibit myocardial contractile force and decrease vascular myogenic activity (e.g., at the arteriolar level). Such inhibitory activity is not observed with flunarizine, which affects Ca2+ entry rather selectively, when calcium overload is imposed upon the vasculature, in particular at cerebrovascular sites. This suggests a potential use of this compound in a number of neurological disorders related to cerebral ischemia.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journal.asp?ref=0077-8923&site=1en_US
dc.relation.ispartofAnnals of the New York Academy of Sciencesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Physiologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.titleCalcium antagonism and vascular smooth muscleen_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.pmid2837122-
dc.identifier.scopuseid_2-s2.0-0023772783en_US
dc.identifier.volume522en_US
dc.identifier.spage234en_US
dc.identifier.epage247en_US
dc.identifier.isiWOS:A1988R662800025-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVan Nueten, JM=7005700327en_US
dc.identifier.scopusauthoridJanssens, WJ=7006876881en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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