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- Publisher Website: 10.1097/00005344-198812006-00007
- Scopus: eid_2-s2.0-0024232142
- PMID: 2468900
- WOS: WOS:A1988T261500007
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Article: Vascular endothelium and Ca2+ antagonists
Title | Vascular endothelium and Ca2+ antagonists |
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Authors | |
Issue Date | 1988 |
Publisher | Lippincott 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? |
Abstract | Endothelial 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 Identifier | http://hdl.handle.net/10722/170908 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.610 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:11:23Z | - |
dc.date.available | 2012-10-30T06:11:23Z | - |
dc.date.issued | 1988 | en_US |
dc.identifier.citation | Journal Of Cardiovascular Pharmacology, 1988, v. 12 SUPPL. 6, p. S21-S28 | en_US |
dc.identifier.issn | 0160-2446 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170908 | - |
dc.description.abstract | Endothelial 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.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ | en_US |
dc.relation.ispartof | Journal of Cardiovascular Pharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Calcium Channel Blockers - Pharmacology | en_US |
dc.subject.mesh | Endothelium, Vascular - Drug Effects - Physiology | en_US |
dc.subject.mesh | Humans | en_US |
dc.title | Vascular endothelium and Ca2+ antagonists | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1097/00005344-198812006-00007 | - |
dc.identifier.pmid | 2468900 | - |
dc.identifier.scopus | eid_2-s2.0-0024232142 | en_US |
dc.identifier.volume | 12 | en_US |
dc.identifier.issue | SUPPL. 6 | en_US |
dc.identifier.spage | S21 | en_US |
dc.identifier.epage | S28 | en_US |
dc.identifier.isi | WOS:A1988T261500007 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0160-2446 | - |