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Article: Inhibition by multivalent cations of contraction induced by Chinese cobra venom cardiotoxin in gunea pig papillary muscle

TitleInhibition by multivalent cations of contraction induced by Chinese cobra venom cardiotoxin in gunea pig papillary muscle
Authors
KeywordsCalcium
Cardiac muscle
Cardiotoxin
Contraction
Snake venom
Issue Date1996
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1996, v. 59 n. 4, p. PL55-PL60 How to Cite?
AbstractThe effects of cardiotoxin (CTX), purified from the venom of Chinese Cobra (Naja naja atra) by a three-step chromatography, on the contractile responses of isolated guinea pig papillary muscle preparation and its antagonism by lanthanum ion (La3+) and divalent cations were examined. CTX induced tonic contraction following a transient augmentation of electrically evoked rhythmic contractions, which is similar to that seen in perfused heart preparation. Multivalent cations, La3+, Ca2+, Mn2+ and Mg2+, concentration-dependently blocked CTX-induced contraction. In Ca2+-free medium, CTX did not induce contraction and CTX-induced contraction was not modified in Na+-free medium. Nifedipine (1 μFull-size image (<1 K)), effectively blocked KC1-induced contracture, but only partially inhibited CTX-induced contraction; thus suggesting that Ca2+ influx induced by CTX utilizes channels other than L-type Ca2+ channels. These cations may compete with CTX for the negatively charged membrane binding site which is responsible for the modulation of Ca2+ movement.
Persistent Identifierhttp://hdl.handle.net/10722/224104
ISSN
2023 Impact Factor: 5.2
2023 SCImago Journal Rankings: 1.257
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, SJ-
dc.contributor.authorKwan, CY-
dc.date.accessioned2016-03-23T08:45:28Z-
dc.date.available2016-03-23T08:45:28Z-
dc.date.issued1996-
dc.identifier.citationLife Sciences, 1996, v. 59 n. 4, p. PL55-PL60-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/224104-
dc.description.abstractThe effects of cardiotoxin (CTX), purified from the venom of Chinese Cobra (Naja naja atra) by a three-step chromatography, on the contractile responses of isolated guinea pig papillary muscle preparation and its antagonism by lanthanum ion (La3+) and divalent cations were examined. CTX induced tonic contraction following a transient augmentation of electrically evoked rhythmic contractions, which is similar to that seen in perfused heart preparation. Multivalent cations, La3+, Ca2+, Mn2+ and Mg2+, concentration-dependently blocked CTX-induced contraction. In Ca2+-free medium, CTX did not induce contraction and CTX-induced contraction was not modified in Na+-free medium. Nifedipine (1 μFull-size image (<1 K)), effectively blocked KC1-induced contracture, but only partially inhibited CTX-induced contraction; thus suggesting that Ca2+ influx induced by CTX utilizes channels other than L-type Ca2+ channels. These cations may compete with CTX for the negatively charged membrane binding site which is responsible for the modulation of Ca2+ movement.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.subjectCalcium-
dc.subjectCardiac muscle-
dc.subjectCardiotoxin-
dc.subjectContraction-
dc.subjectSnake venom-
dc.subject.meshCations - pharmacology-
dc.subject.meshCobra Cardiotoxin Proteins - isolation & purification - pharmacology-
dc.subject.meshMuscle Contraction - drug effects-
dc.subject.meshPapillary Muscles - drug effects - physiology-
dc.subject.meshPotassium Chloride - pharmacology-
dc.titleInhibition by multivalent cations of contraction induced by Chinese cobra venom cardiotoxin in gunea pig papillary muscle-
dc.typeArticle-
dc.identifier.emailKwan, DCY: cykwan@hkucc.hku.hk-
dc.identifier.doi10.1016/0024-3205(96)00305-0-
dc.identifier.pmid8761008-
dc.identifier.scopuseid_2-s2.0-0030036411-
dc.identifier.hkuros27009-
dc.identifier.volume59-
dc.identifier.issue4-
dc.identifier.spagePL55-
dc.identifier.epagePL60-
dc.identifier.isiWOS:A1996UT66500010-
dc.publisher.placeUnited States-
dc.identifier.issnl0024-3205-

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