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Article: Role of calcium and endothelium in hypertension, cardiovascular disease, and subsequent vascular events

TitleRole of calcium and endothelium in hypertension, cardiovascular disease, and subsequent vascular events
Authors
Issue Date1992
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1992, v. 19 SUPPL. 3, p. S6-S10 How to Cite?
AbstractThe response of isolated blood vessels to vasoactive agonists is modulated by endothelial cells. Nitric oxide is probably the major endothelium-derived relaxing factor (EDRF), although an unidentified hyperpolarizing factor and prostacyclin are secreted. Previous studies indicate that the release of EDRF must require an increase in cytoplasmic calcium in the endothelial cells. In perfused arteries, calcium-channel activators also trigger the release of EDRF; thus, the endothelial cell membrane must contain voltage-operated calcium channels. However, the increase in cytoplasmic calcium stimulating EDRF release is not due to activation of these channels. Endothelial cells also release constricting factors (EDCF), most likely superoxide anions, endoperoxides, and endothelin. Endothelium-dependent contractions can be evoked by anoxia. These contractions, as well as the endothelium-dependent increases in tension evoked by stretch in cerebral arteries, are inhibited by calcium antagonists. This inhibitory effect is at the level of vascular smooth muscle, not the endothelium. Thus, calcium antagonists do not prevent the release of either EDRF or EDCF. Indeed, by facilitating the inhibition exerted by the former and preventing the activation of vascular smooth muscle by the latter, they favor dilation.
Persistent Identifierhttp://hdl.handle.net/10722/171058
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.accessioned2012-10-30T06:12:01Z-
dc.date.available2012-10-30T06:12:01Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1992, v. 19 SUPPL. 3, p. S6-S10en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171058-
dc.description.abstractThe response of isolated blood vessels to vasoactive agonists is modulated by endothelial cells. Nitric oxide is probably the major endothelium-derived relaxing factor (EDRF), although an unidentified hyperpolarizing factor and prostacyclin are secreted. Previous studies indicate that the release of EDRF must require an increase in cytoplasmic calcium in the endothelial cells. In perfused arteries, calcium-channel activators also trigger the release of EDRF; thus, the endothelial cell membrane must contain voltage-operated calcium channels. However, the increase in cytoplasmic calcium stimulating EDRF release is not due to activation of these channels. Endothelial cells also release constricting factors (EDCF), most likely superoxide anions, endoperoxides, and endothelin. Endothelium-dependent contractions can be evoked by anoxia. These contractions, as well as the endothelium-dependent increases in tension evoked by stretch in cerebral arteries, are inhibited by calcium antagonists. This inhibitory effect is at the level of vascular smooth muscle, not the endothelium. Thus, calcium antagonists do not prevent the release of either EDRF or EDCF. Indeed, by facilitating the inhibition exerted by the former and preventing the activation of vascular smooth muscle by the latter, they favor dilation.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.meshCalcium - Pharmacologyen_US
dc.subject.meshCardiovascular Diseases - Etiologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension - Etiologyen_US
dc.titleRole of calcium and endothelium in hypertension, cardiovascular disease, and subsequent vascular eventsen_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.pmid1376838-
dc.identifier.scopuseid_2-s2.0-0026631512en_US
dc.identifier.volume19en_US
dc.identifier.issueSUPPL. 3en_US
dc.identifier.spageS6en_US
dc.identifier.epageS10en_US
dc.identifier.isiWOS:A1992HX76000003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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