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Article: Vascular endothelium and Ca2+ antagonists

TitleVascular endothelium and Ca2+ antagonists
Authors
Issue Date1988
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1988, v. 12 SUPPL. 6, p. S21-S28 How to Cite?
AbstractEndothelial cells can release both relaxing and contracting factors. Since the release of endothelium-dependent relaxing factor is prevented by incubation of Ca2+-free solution and can be triggered by the Ca2+ ionophore A 23187, it must require an increase in cytoplasmic Ca2+ concentration in the endothelial cells. Ca2+-channel agonists also evoke the release of endothelium-dependent relaxing factor, an effect prevented by dihydropyridines; thus, the endothelial cell membrane must contain voltage-operated Ca2+ channels. However, since verapamil and dihydropyridines do not prevent the release of endothelium-dependent relaxing factor evoked by acetylcholine, the increase in cytoplasmic Ca2+ concentration leading to the release of the mediator is not due to activation of these channels. Diltiazem has an inhibitory effect on the release of endothelium-dependent relaxing factor, which cannot be attributed to the action of the compound at Ca2+ channels. In the presence of functional endothelium, endothelium-dependent relaxing factor and Ca2+ antagonist such as nisoldipine are synergistic in inhibiting contractions of vascular smooth muscle. In a variety of arteries and veins, 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, can be inhibited by Ca2+ antagonists. In the aorta of the spontaneously hypertensive rat, acetylcholine causes endothelium-dependent contractions, an effect that is inhibited by diltiazem. To judge from experiments in anoxic coronary arteries, the inhibitory effect of Ca2+ antagonists on endothelium-dependent contractions is at the level of the vascular smooth muscle, and not the endothelium. Thus, Ca2+ antagonists do not prevent the release of either endothelium-dependent relaxing factor or endothelium-dependent contracting factor; by facilitating the inhibition exerted by the former, and preventing the activation of vascular smooth muscle by the latter, they favor the occurrence of dilatation.
Persistent Identifierhttp://hdl.handle.net/10722/170908
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.accessioned2012-10-30T06:11:23Z-
dc.date.available2012-10-30T06:11:23Z-
dc.date.issued1988en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1988, v. 12 SUPPL. 6, p. S21-S28en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170908-
dc.description.abstractEndothelial cells can release both relaxing and contracting factors. Since the release of endothelium-dependent relaxing factor is prevented by incubation of Ca2+-free solution and can be triggered by the Ca2+ ionophore A 23187, it must require an increase in cytoplasmic Ca2+ concentration in the endothelial cells. Ca2+-channel agonists also evoke the release of endothelium-dependent relaxing factor, an effect prevented by dihydropyridines; thus, the endothelial cell membrane must contain voltage-operated Ca2+ channels. However, since verapamil and dihydropyridines do not prevent the release of endothelium-dependent relaxing factor evoked by acetylcholine, the increase in cytoplasmic Ca2+ concentration leading to the release of the mediator is not due to activation of these channels. Diltiazem has an inhibitory effect on the release of endothelium-dependent relaxing factor, which cannot be attributed to the action of the compound at Ca2+ channels. In the presence of functional endothelium, endothelium-dependent relaxing factor and Ca2+ antagonist such as nisoldipine are synergistic in inhibiting contractions of vascular smooth muscle. In a variety of arteries and veins, 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, can be inhibited by Ca2+ antagonists. In the aorta of the spontaneously hypertensive rat, acetylcholine causes endothelium-dependent contractions, an effect that is inhibited by diltiazem. To judge from experiments in anoxic coronary arteries, the inhibitory effect of Ca2+ antagonists on endothelium-dependent contractions is at the level of the vascular smooth muscle, and not the endothelium. Thus, Ca2+ antagonists do not prevent the release of either endothelium-dependent relaxing factor or endothelium-dependent contracting factor; by facilitating the inhibition exerted by the former, and preventing the activation of vascular smooth muscle by the latter, they favor the occurrence of dilatation.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.meshAnimalsen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshHumansen_US
dc.titleVascular endothelium and Ca2+ antagonistsen_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.doi10.1097/00005344-198812006-00007-
dc.identifier.pmid2468900-
dc.identifier.scopuseid_2-s2.0-0024232142en_US
dc.identifier.volume12en_US
dc.identifier.issueSUPPL. 6en_US
dc.identifier.spageS21en_US
dc.identifier.epageS28en_US
dc.identifier.isiWOS:A1988T261500007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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