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Article: Endothelium-dependent contractions to acetylcholine, ATP and the calcium ionophore A 23187 in aortas from spontaneously hypertensive and normotensive rats

TitleEndothelium-dependent contractions to acetylcholine, ATP and the calcium ionophore A 23187 in aortas from spontaneously hypertensive and normotensive rats
Authors
KeywordsEndothelium-dependent contraction
Endothelium-derived contracting factor
Intracellular concentration of calcium
Spontaneously hypertensive rat
Issue Date2004
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/FCP
Citation
Fundamental And Clinical Pharmacology, 2004, v. 18 n. 3, p. 321-326 How to Cite?
AbstractThe present study was designed to determine whether or not an increase in endothelial intracellular concentration of calcium ([Ca2+] i) evokes endothelium-dependent contractions in the aorta from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine, adenosine triphosphate (ATP) and the calcium ionophore, A 23187, produced endothelium-dependent relaxations in isolated aortic rings of both WKY and SHR. These relaxations in response to the three agonists were significantly smaller in the SHR when compared with the WKY. Endothelium-dependent contractions to acetylcholine, ATP and A 23187 were observed only in the aorta isolated from the SHR. In the presence of NG-nitro-L-arginine, an NO synthase inhibitor, the endothelium-dependent contractions in response to acetylcholine, ATP and A 23187 were potentiated significantly in the aorta SHR and were unmasked in that of WKY. However, the contractions were still significantly greater in SHR than in WKY. These contractions were abolished by indomethacin and valeryl salicylate (two cyclo-oxygenase inhibitors) as well as by S 18886 (a TP-receptor antagonist), indicating that the endothelium-dependent contraction produced by the three agonists share the same characteristics. The results of the present study indicate that the release/generation of endothelium-derived contracting factor, requires an increase in endothelial [Ca2+]i.
Persistent Identifierhttp://hdl.handle.net/10722/80280
ISSN
2023 Impact Factor: 2.1
2023 SCImago Journal Rankings: 0.586
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Den_HK
dc.contributor.authorGluais, Pen_HK
dc.contributor.authorZhang, JNen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorFélétou, Men_HK
dc.date.accessioned2010-09-06T08:04:33Z-
dc.date.available2010-09-06T08:04:33Z-
dc.date.issued2004en_HK
dc.identifier.citationFundamental And Clinical Pharmacology, 2004, v. 18 n. 3, p. 321-326en_HK
dc.identifier.issn0767-3981en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80280-
dc.description.abstractThe present study was designed to determine whether or not an increase in endothelial intracellular concentration of calcium ([Ca2+] i) evokes endothelium-dependent contractions in the aorta from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine, adenosine triphosphate (ATP) and the calcium ionophore, A 23187, produced endothelium-dependent relaxations in isolated aortic rings of both WKY and SHR. These relaxations in response to the three agonists were significantly smaller in the SHR when compared with the WKY. Endothelium-dependent contractions to acetylcholine, ATP and A 23187 were observed only in the aorta isolated from the SHR. In the presence of NG-nitro-L-arginine, an NO synthase inhibitor, the endothelium-dependent contractions in response to acetylcholine, ATP and A 23187 were potentiated significantly in the aorta SHR and were unmasked in that of WKY. However, the contractions were still significantly greater in SHR than in WKY. These contractions were abolished by indomethacin and valeryl salicylate (two cyclo-oxygenase inhibitors) as well as by S 18886 (a TP-receptor antagonist), indicating that the endothelium-dependent contraction produced by the three agonists share the same characteristics. The results of the present study indicate that the release/generation of endothelium-derived contracting factor, requires an increase in endothelial [Ca2+]i.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/FCPen_HK
dc.relation.ispartofFundamental and Clinical Pharmacologyen_HK
dc.rightsFundamental and Clinical Pharmacology. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectEndothelium-dependent contractionen_HK
dc.subjectEndothelium-derived contracting factoren_HK
dc.subjectIntracellular concentration of calciumen_HK
dc.subjectSpontaneously hypertensive raten_HK
dc.titleEndothelium-dependent contractions to acetylcholine, ATP and the calcium ionophore A 23187 in aortas from spontaneously hypertensive and normotensive ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0767-3981&volume=18&spage=321&epage=326&date=2004&atitle=Endothelium-dependent+contractions+to+acetylcholine,+ATP+and+the+calcium+ionophore+A+23187+in+aortas+from+spontaneously+hypertensive+and+normotensive+ratsen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1472-8206.2004.00247.xen_HK
dc.identifier.pmid15147283en_HK
dc.identifier.scopuseid_2-s2.0-2942572772en_HK
dc.identifier.hkuros88576en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2942572772&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume18en_HK
dc.identifier.issue3en_HK
dc.identifier.spage321en_HK
dc.identifier.epage326en_HK
dc.identifier.isiWOS:000221949100006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYang, D=7404801018en_HK
dc.identifier.scopusauthoridGluais, P=6602456462en_HK
dc.identifier.scopusauthoridZhang, JN=7601344287en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.issnl0767-3981-

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