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Article: Dual effect of cobra cardiotoxin on vascular smooth muscle and endothelium

TitleDual effect of cobra cardiotoxin on vascular smooth muscle and endothelium
Authors
Issue Date1998
PublisherNature Publishing Group.
Citation
Acta Pharmacologica Sinica, 1998, v. 19 n. 3, p. 197-202 How to Cite?
AbstractAIM: To assess the cytotoxic effects of cobra cardiotoxin (CTX) on rat aorta. METHODS: Measure of contractility of aortic rings with or without endothelium. RESULTS: In endothelium-intact rings, CTX 10 μmol · L -1 induced a transient relaxation followed by a sustained contraction. Removal of the endothelium or preincubation of the rings with NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) abolished the transient relaxation but did not affect the magnitude of the contractile response induced by CTX. CTX itself induced contraction of vascular smooth muscle but also reduced contractions induced by phenylephrine (PhE) or KCl stimulation in a concentration-dependent manner. Contraction induced by CTX was dependent on the external Ca 2+ concentration. Maximal contractile response to CTX was obtained in medium containing Ca 2+ 1 mmol · L -1. This response decreased with higher Ca 2+ concentration and disappeared when Ca 2+ 7 mmol · L - 1, organic and inorganic calcium channel blockers were present in the external solution before CTX addition. In preparations with the endothelium intact and incubated with CYX, relaxation by acetylcholine (ACh) stimulation of the tension induced by PhE was decreased. Endothelium-dependent relaxation to ACh was preserved when Ca 2+ 5 mmol · L -1 was added to the medium prior to CTX. CONCLUSION: CTX first triggers the release of NO from the endothelium which results in muscle relaxation, and then causes smooth muscle contraction. Ca 2+ and Ca 2+ channel blockers prevented the effect of CTX.
Persistent Identifierhttp://hdl.handle.net/10722/81334
ISSN
2000 Impact Factor: 0.485
References

 

DC FieldValueLanguage
dc.contributor.authorHo, KHen_HK
dc.contributor.authorKwan, CYen_HK
dc.contributor.authorHuang, SJen_HK
dc.contributor.authorBourreau, JPen_HK
dc.date.accessioned2010-09-06T08:16:28Z-
dc.date.available2010-09-06T08:16:28Z-
dc.date.issued1998en_HK
dc.identifier.citationActa Pharmacologica Sinica, 1998, v. 19 n. 3, p. 197-202en_HK
dc.identifier.issn0253-9756en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81334-
dc.description.abstractAIM: To assess the cytotoxic effects of cobra cardiotoxin (CTX) on rat aorta. METHODS: Measure of contractility of aortic rings with or without endothelium. RESULTS: In endothelium-intact rings, CTX 10 μmol · L -1 induced a transient relaxation followed by a sustained contraction. Removal of the endothelium or preincubation of the rings with NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) abolished the transient relaxation but did not affect the magnitude of the contractile response induced by CTX. CTX itself induced contraction of vascular smooth muscle but also reduced contractions induced by phenylephrine (PhE) or KCl stimulation in a concentration-dependent manner. Contraction induced by CTX was dependent on the external Ca 2+ concentration. Maximal contractile response to CTX was obtained in medium containing Ca 2+ 1 mmol · L -1. This response decreased with higher Ca 2+ concentration and disappeared when Ca 2+ 7 mmol · L - 1, organic and inorganic calcium channel blockers were present in the external solution before CTX addition. In preparations with the endothelium intact and incubated with CYX, relaxation by acetylcholine (ACh) stimulation of the tension induced by PhE was decreased. Endothelium-dependent relaxation to ACh was preserved when Ca 2+ 5 mmol · L -1 was added to the medium prior to CTX. CONCLUSION: CTX first triggers the release of NO from the endothelium which results in muscle relaxation, and then causes smooth muscle contraction. Ca 2+ and Ca 2+ channel blockers prevented the effect of CTX.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group.en_HK
dc.relation.ispartofActa Pharmacologica Sinicaen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAorta, Thoracic - drug effectsen_HK
dc.subject.meshCalcium Channel Blockers - pharmacologyen_HK
dc.subject.meshCobra Cardiotoxin Proteins - toxicityen_HK
dc.subject.meshEndothelium, Vascular - physiologyen_HK
dc.subject.meshMuscle Contraction - drug effectsen_HK
dc.subject.meshMuscle, Smooth, Vascular - drug effectsen_HK
dc.subject.meshNG-Nitroarginine Methyl Ester - pharmacologyen_HK
dc.subject.meshNitric Oxide Synthase - antagonists & inhibitorsen_HK
dc.subject.meshPhenylephrine - pharmacologyen_HK
dc.subject.meshPotassium Chloride - pharmacologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshVasoconstrictor Agents - pharmacologyen_HK
dc.titleDual effect of cobra cardiotoxin on vascular smooth muscle and endotheliumen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1671-4083&volume=19&issue=3&spage=197&epage=202&date=1998&atitle=Dual+effect+of+Cobra+cardiotoxin+on+vascular+smooth+muscle+and+endotheliumen_HK
dc.identifier.emailBourreau, JP: bourreau@hkucc.hku.hken_HK
dc.identifier.authorityBourreau, JP=rp00389en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10375725-
dc.identifier.scopuseid_2-s2.0-0031836629en_HK
dc.identifier.hkuros36791en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031836629&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue3en_HK
dc.identifier.spage197en_HK
dc.identifier.epage202en_HK
dc.identifier.scopusauthoridHo, KH=55205630300en_HK
dc.identifier.scopusauthoridKwan, CY=7201421224en_HK
dc.identifier.scopusauthoridHuang, SJ=7405417684en_HK
dc.identifier.scopusauthoridBourreau, JP=7003927886en_HK

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