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Article: Calcium and reactive oxygen species increase in endothelial cells in response to releasers of endothelium-derived contracting factor

TitleCalcium and reactive oxygen species increase in endothelial cells in response to releasers of endothelium-derived contracting factor
Authors
KeywordsCalcium dysfunction
Endothelium-derived contracting factors
Reactive oxygen species
Spontaneously hypertensive rats
Issue Date2007
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2007, v. 151 n. 1, p. 15-23 How to Cite?
AbstractBackground and Purpose: Experiments were designed to assess whether or not the intracellular concentration of calcium and reactive oxygen species (ROS) increase in endothelial cells of the rat thoracic aorta in response to releasers of endothelium-derived contracting factor (EDCF) and if so, whether or not a difference exists between spontaneously hypertensive (SHR) and normotensive (WKY) rats. Experimental approach: Calcium and ROS were measured by confocal microscopy, using Fura-red in combination with Fluo-4 and dichlorodihydrofluorescein diacetate, respectively. Key results: Acetylcholine caused a rapid increase in cytosolic calcium concentration in endothelial cells of both SHR and WKY, which was significantly more pronounced in aortae of the former strain. This rise of calcium was not affected by indomethacin (an inhibitor of cyclooxygenase) or Tiron plus diethyldithiocarbamate acid (DETCA) (membrane permeable antioxidants). In the presence of a nitric oxide synthase blocker, acetylcholine also caused a rapid increase in ROS in endothelial cells of SHR but not in those of WKY. The burst of ROS was prevented by indomethacin or Tiron plus DETCA. Conclusions and implications: These experiments show that endothelial cells of SHR are more prone to calcium and ROS overload upon stimulation with acetylcholine. The abnormal accumulation of calcium is a prerequisite to initiate the release of EDCF and can be mimicked using the calcium ionophore A23187. The sequence of events occurring during endothelium-dependent contractions firstly requires the accumulation of calcium, which then activates cyclooxygenase and produces ROS along with EDCF that in turn stimulates TP-receptors, resulting in EDCF-mediated contractions. © 2007 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67453
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorLeung, FPen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorFeletou, Men_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T05:55:16Z-
dc.date.available2010-09-06T05:55:16Z-
dc.date.issued2007en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2007, v. 151 n. 1, p. 15-23en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67453-
dc.description.abstractBackground and Purpose: Experiments were designed to assess whether or not the intracellular concentration of calcium and reactive oxygen species (ROS) increase in endothelial cells of the rat thoracic aorta in response to releasers of endothelium-derived contracting factor (EDCF) and if so, whether or not a difference exists between spontaneously hypertensive (SHR) and normotensive (WKY) rats. Experimental approach: Calcium and ROS were measured by confocal microscopy, using Fura-red in combination with Fluo-4 and dichlorodihydrofluorescein diacetate, respectively. Key results: Acetylcholine caused a rapid increase in cytosolic calcium concentration in endothelial cells of both SHR and WKY, which was significantly more pronounced in aortae of the former strain. This rise of calcium was not affected by indomethacin (an inhibitor of cyclooxygenase) or Tiron plus diethyldithiocarbamate acid (DETCA) (membrane permeable antioxidants). In the presence of a nitric oxide synthase blocker, acetylcholine also caused a rapid increase in ROS in endothelial cells of SHR but not in those of WKY. The burst of ROS was prevented by indomethacin or Tiron plus DETCA. Conclusions and implications: These experiments show that endothelial cells of SHR are more prone to calcium and ROS overload upon stimulation with acetylcholine. The abnormal accumulation of calcium is a prerequisite to initiate the release of EDCF and can be mimicked using the calcium ionophore A23187. The sequence of events occurring during endothelium-dependent contractions firstly requires the accumulation of calcium, which then activates cyclooxygenase and produces ROS along with EDCF that in turn stimulates TP-receptors, resulting in EDCF-mediated contractions. © 2007 Nature Publishing Group All rights reserved.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectCalcium dysfunctionen_HK
dc.subjectEndothelium-derived contracting factorsen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subjectSpontaneously hypertensive ratsen_HK
dc.titleCalcium and reactive oxygen species increase in endothelial cells in response to releasers of endothelium-derived contracting factoren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=151&issue=1&spage=15&epage=23&date=2007&atitle=Calcium+and+rea+tive+oxygen+species+increase+in+endothelial+cells+in+response+to+releasers+of+endothelium-derived+contracting+factoren_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/sj.bjp.0707190en_HK
dc.identifier.pmid17351662en_HK
dc.identifier.pmcidPMC2012974-
dc.identifier.scopuseid_2-s2.0-34247608691en_HK
dc.identifier.hkuros135184en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247608691&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume151en_HK
dc.identifier.issue1en_HK
dc.identifier.spage15en_HK
dc.identifier.epage23en_HK
dc.identifier.isiWOS:000246230100002-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridLeung, FP=8615375300en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK
dc.identifier.scopusauthoridFeletou, M=7006461826en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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