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Article: Calcium and activation of the release of endothelium-derived relaxing factor

TitleCalcium and activation of the release of endothelium-derived relaxing factor
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. 226-233 How to Cite?
AbstractIndirect and direct experimental evidence demonstrates that both the entry of extracellular calcium and the liberation of calcium from intracellular stores can contribute to an increase in free cytoplasmic calcium concentration in endothelial cells, which seems to be an essential step in the synthesis and/or release of endothelium-derived relaxing factor(s). A variety of Ca2+ transport mechanisms may be involved in the regulation of cytoplasmic calcium in endothelial cells. Ca2+ entry may occur via voltage-operated Ca2+ channels. If they do exist, these channels may have characteristics different from those in underlying vascular smooth muscle cells. Sustained activation of the release of EDRF by various receptor agonists (e.g., acetylcholine, adenine nucleotides, and bradykinin) is also dependent on Ca2+ entry, but it is insensitive to organic Ca2+ channel antagonists. These findings indicate that, when used clinically in various cardiovascular diseases, organic calcium channel antagonists are not expected to interfere with endothelium-dependent relaxation evoked by endogenous vasoactive substances (e.g., ADP, serotonin). Since amiloride and its analogues blocked endothelium-dependent relaxations in different arterial preparations, Na+ transport and Na+/Ca2+ exchange were suggested to play a role in calcium-dependent release of EDRF. The exact nature of Ca2+ transport mechanisms and also the calcium-sensitive cellular processes that lead to the synthesis/release of endothelium derived relaxing factor(s) remain to be determined. However, the available data suggest that calcium handling by the vascular smooth muscle and endothelial cells may be different, allowing potentially selective modulation of Ca2+ activtion in these two cell types.
Persistent Identifierhttp://hdl.handle.net/10722/170878
ISSN
2015 Impact Factor: 4.518
2015 SCImago Journal Rankings: 2.389
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, GMen_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. 226-233en_US
dc.identifier.issn0077-8923en_US
dc.identifier.urihttp://hdl.handle.net/10722/170878-
dc.description.abstractIndirect and direct experimental evidence demonstrates that both the entry of extracellular calcium and the liberation of calcium from intracellular stores can contribute to an increase in free cytoplasmic calcium concentration in endothelial cells, which seems to be an essential step in the synthesis and/or release of endothelium-derived relaxing factor(s). A variety of Ca2+ transport mechanisms may be involved in the regulation of cytoplasmic calcium in endothelial cells. Ca2+ entry may occur via voltage-operated Ca2+ channels. If they do exist, these channels may have characteristics different from those in underlying vascular smooth muscle cells. Sustained activation of the release of EDRF by various receptor agonists (e.g., acetylcholine, adenine nucleotides, and bradykinin) is also dependent on Ca2+ entry, but it is insensitive to organic Ca2+ channel antagonists. These findings indicate that, when used clinically in various cardiovascular diseases, organic calcium channel antagonists are not expected to interfere with endothelium-dependent relaxation evoked by endogenous vasoactive substances (e.g., ADP, serotonin). Since amiloride and its analogues blocked endothelium-dependent relaxations in different arterial preparations, Na+ transport and Na+/Ca2+ exchange were suggested to play a role in calcium-dependent release of EDRF. The exact nature of Ca2+ transport mechanisms and also the calcium-sensitive cellular processes that lead to the synthesis/release of endothelium derived relaxing factor(s) remain to be determined. However, the available data suggest that calcium handling by the vascular smooth muscle and endothelial cells may be different, allowing potentially selective modulation of Ca2+ activtion in these two cell types.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.meshBiological Agents - Secretionen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channel Agonists - Pharmacologyen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshRabbitsen_US
dc.subject.meshSodium - Metabolismen_US
dc.titleCalcium and activation of the release of endothelium-derived relaxing factoren_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.doi10.1111/j.1749-6632.1988.tb33360.x-
dc.identifier.pmid3288050-
dc.identifier.scopuseid_2-s2.0-0023759480en_US
dc.identifier.volume522en_US
dc.identifier.spage226en_US
dc.identifier.epage233en_US
dc.identifier.isiWOS:A1988R662800024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, GM=7005517991en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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