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Article: Cobra cardiotoxin induced initial transient relaxation followed by contraction in rat aortic rings

TitleCobra cardiotoxin induced initial transient relaxation followed by contraction in rat aortic rings
Authors
Issue Date1996
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 1996, v. 10 n. 3, p. A440 How to Cite?
AbstractThe mechanism of actions of cardiotoxin (CTX), a basic polypeptide purified chronutographically from cobra venom, on vascular contraction was investigated. CTX (10 μM)-induced small, variable and transient relaxation in endothelnim-intact aortic rings followed by large, consistent and sustained contraction. Rings precontracted with 1 μM phenylephrme (PE) showed substantial transient relaxation when CTX was added to the plateau phase of the PE-contraction. Pre-incubation of rings with L-NAME (NO synthase inhibitor) inhibited the relaxation indicating NO is responsible for the relaxation. CTX also caused contraction in Ca 2+-dependent manner with maximal contractile force at 0.5 mM but high CV 2+ (7 mM) totally inhibited the CTX-induced contraction. The CTX inducedcontraction in endothelhun-intact and -denuded aortic rings showed no difference in maximal tension development indicating the loss of functional endothelial cells following CTX treatment. ACh-induced relaxation was lost after CTX treatment but was retained partially when high Ca 2+ was present prior to the addition of CTX. Not only high Ca 2+ could inhibit the CTX-induced contraction so did Ni 2+, Tetrandrine, SK&F 96365 and Nifedipine. Hence, we conclude that CTX triggers the release of MO from the damaged endothelitun and the subsequent contractile response is probably due to enhanced membrane leak to Co 2+ in damaged smooth muscle cells. High Co 2+ and other Co 2+ antagonists protect endothelial and smooth muscle cells from CTX-induced damage via its action on Co 2+-channels and Co 2+-binding site. (Supported by HKRGC).
Persistent Identifierhttp://hdl.handle.net/10722/171735
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorHo, KHen_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorHuang, SJen_US
dc.contributor.authorBourreau, JPen_US
dc.date.accessioned2012-10-30T06:16:41Z-
dc.date.available2012-10-30T06:16:41Z-
dc.date.issued1996en_US
dc.identifier.citationFaseb Journal, 1996, v. 10 n. 3, p. A440en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10722/171735-
dc.description.abstractThe mechanism of actions of cardiotoxin (CTX), a basic polypeptide purified chronutographically from cobra venom, on vascular contraction was investigated. CTX (10 μM)-induced small, variable and transient relaxation in endothelnim-intact aortic rings followed by large, consistent and sustained contraction. Rings precontracted with 1 μM phenylephrme (PE) showed substantial transient relaxation when CTX was added to the plateau phase of the PE-contraction. Pre-incubation of rings with L-NAME (NO synthase inhibitor) inhibited the relaxation indicating NO is responsible for the relaxation. CTX also caused contraction in Ca 2+-dependent manner with maximal contractile force at 0.5 mM but high CV 2+ (7 mM) totally inhibited the CTX-induced contraction. The CTX inducedcontraction in endothelhun-intact and -denuded aortic rings showed no difference in maximal tension development indicating the loss of functional endothelial cells following CTX treatment. ACh-induced relaxation was lost after CTX treatment but was retained partially when high Ca 2+ was present prior to the addition of CTX. Not only high Ca 2+ could inhibit the CTX-induced contraction so did Ni 2+, Tetrandrine, SK&F 96365 and Nifedipine. Hence, we conclude that CTX triggers the release of MO from the damaged endothelitun and the subsequent contractile response is probably due to enhanced membrane leak to Co 2+ in damaged smooth muscle cells. High Co 2+ and other Co 2+ antagonists protect endothelial and smooth muscle cells from CTX-induced damage via its action on Co 2+-channels and Co 2+-binding site. (Supported by HKRGC).en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_US
dc.relation.ispartofFASEB Journalen_US
dc.titleCobra cardiotoxin induced initial transient relaxation followed by contraction in rat aortic ringsen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-25344456644en_US
dc.identifier.volume10en_US
dc.identifier.issue3en_US
dc.identifier.spageA440en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHo, KH=55205630300en_US
dc.identifier.scopusauthoridKwan, CY=7201421224en_US
dc.identifier.scopusauthoridHuang, SJ=7405417684en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US

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