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Article: Modulation of cardiac Na+ current by gadolinium, a blocker of stretch-induced arrhythmias

TitleModulation of cardiac Na+ current by gadolinium, a blocker of stretch-induced arrhythmias
Authors
Issue Date2001
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2001, v. 280 n. 1 49-1, p. H272-H279 How to Cite?
AbstractGd3+ blocks stretch-activated channels and suppresses stretch-induced arrhythmias. We used whole cell voltage clamp to examine whether effects on Na+ channel might contribute to the antiarrhythmic efficacy of Gd3+ Gd3+ inhibited Na′ current (INa) in rabbit ventricle (IC50 = 48 μM at -35 mV, holding potential -120 mV), and block increased at more negative test potentials. Gd3+ made the threshold for INa more positive and reduced the maximum con tuctance. Gd3+ (50 μM) shifted the midpoints for activation and inactivation of INa 7.9 and 5.7 mV positive but did not alter the slope factor for either relationship. Activation and inactivation kinetics were slowed in a manner that could not be explained solely by altered surface potential. Paradoxically, Gd3+ increased INa under certain conditions. With membrane potential held at -75 mV, Gd3+ still shifted threshold for activation positive, but INa increased positive to -40 mV, causing the current-voltage curves to cross over. When availability initially was low, increased availability induced by Gd3+ dominated the response at test potentials positive to -40 mV. The results indicate that Gd3+ has complex effects on cardiac Na+ channels. Independent of holding potential, Gd3+ is a potent INa blocker near threshold potential, and inhibition of INa by Gd3+ is likely to contribute to suppression of stretch-induced arrhythmias.
Persistent Identifierhttp://hdl.handle.net/10722/162493
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_US
dc.contributor.authorBaumgarten, CMen_US
dc.date.accessioned2012-09-05T05:20:30Z-
dc.date.available2012-09-05T05:20:30Z-
dc.date.issued2001en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2001, v. 280 n. 1 49-1, p. H272-H279en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/162493-
dc.description.abstractGd3+ blocks stretch-activated channels and suppresses stretch-induced arrhythmias. We used whole cell voltage clamp to examine whether effects on Na+ channel might contribute to the antiarrhythmic efficacy of Gd3+ Gd3+ inhibited Na′ current (INa) in rabbit ventricle (IC50 = 48 μM at -35 mV, holding potential -120 mV), and block increased at more negative test potentials. Gd3+ made the threshold for INa more positive and reduced the maximum con tuctance. Gd3+ (50 μM) shifted the midpoints for activation and inactivation of INa 7.9 and 5.7 mV positive but did not alter the slope factor for either relationship. Activation and inactivation kinetics were slowed in a manner that could not be explained solely by altered surface potential. Paradoxically, Gd3+ increased INa under certain conditions. With membrane potential held at -75 mV, Gd3+ still shifted threshold for activation positive, but INa increased positive to -40 mV, causing the current-voltage curves to cross over. When availability initially was low, increased availability induced by Gd3+ dominated the response at test potentials positive to -40 mV. The results indicate that Gd3+ has complex effects on cardiac Na+ channels. Independent of holding potential, Gd3+ is a potent INa blocker near threshold potential, and inhibition of INa by Gd3+ is likely to contribute to suppression of stretch-induced arrhythmias.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAlgorithmsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Arrhythmia Agents - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGadolinium - Pharmacologyen_US
dc.subject.meshHeart - Drug Effects - Physiologyen_US
dc.subject.meshHeart Ventricles - Drug Effectsen_US
dc.subject.meshKineticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMyocardium - Cytology - Metabolismen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshRabbitsen_US
dc.subject.meshSodium Channel Blockersen_US
dc.subject.meshSodium Channels - Metabolismen_US
dc.subject.meshStress, Mechanicalen_US
dc.titleModulation of cardiac Na+ current by gadolinium, a blocker of stretch-induced arrhythmiasen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11123242-
dc.identifier.scopuseid_2-s2.0-0035021649en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035021649&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume280en_US
dc.identifier.issue1 49-1en_US
dc.identifier.spageH272en_US
dc.identifier.epageH279en_US
dc.identifier.isiWOS:000165948500032-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridBaumgarten, CM=7006283434en_US

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