File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effects of RP58866 on transmembrane K + currents in mammalian ventricular myocytes

TitleEffects of RP58866 on transmembrane K + currents in mammalian ventricular myocytes
Authors
Issue Date1999
Citation
Acta Pharmacologica Sinica, 1999, v. 20 n. 11, p. 961-969 How to Cite?
AbstractAIM: To determine effects of RP58866 on inward rectifier K + current (I(Kl)), transient outward K + current (I(to)) and delayed outward rectifier K + current (I(K)) in isolated cardiac myocytes. METHODS: In isolated ventricular myocytes of guinea pig and dog, the effect of RP58866 on I(Kl), I(to), and I(K) were observed by the whole cell voltage-clamp technique. RESULTS: RP58866 decreased I(Kl) in a concentration-dependent manner, with an IC 50 of (3.4 ± 0.8) μmol · L -1 (n = 6) at -100 mV in guinea pig ventricular cells. In dog ventricular myocytes, RP58866 inhibited I(to) with IC 50 of (2.3 ± 0.5) μmol · L -1 at +40 mV. In guinea pig ventricular cells, RP58866 at 100 μmol · L -1 decreased I(K): I(Kstep) by (58 ± 13)% at +40 mV, and I(Ktail) by (86 ± 17)%, respectively. RP58866 inhibited I(Kstep) with an IC 50 of (7.5 ± 0.8) μmol · L -1, and I(Ktail) with an IC 50 of (3.5 ± 0.9) μmol · L -1. The envelope of tail analysis suggested that both I(Kr) and I(Ks) were inhibited. CONCLUSION: RP58866 inhibits I(Kl), I(to), and I(K) in cardiac myocytes with a similar potency, and is not a specific I(Kl) inhibitor.
Persistent Identifierhttp://hdl.handle.net/10722/162292
ISSN
2000 Impact Factor: 0.485
References

 

DC FieldValueLanguage
dc.contributor.authorYang, BFen_US
dc.contributor.authorLi, GRen_US
dc.contributor.authorXu, CQen_US
dc.contributor.authorNattel, Sen_US
dc.date.accessioned2012-09-05T05:18:42Z-
dc.date.available2012-09-05T05:18:42Z-
dc.date.issued1999en_US
dc.identifier.citationActa Pharmacologica Sinica, 1999, v. 20 n. 11, p. 961-969en_US
dc.identifier.issn0253-9756en_US
dc.identifier.urihttp://hdl.handle.net/10722/162292-
dc.description.abstractAIM: To determine effects of RP58866 on inward rectifier K + current (I(Kl)), transient outward K + current (I(to)) and delayed outward rectifier K + current (I(K)) in isolated cardiac myocytes. METHODS: In isolated ventricular myocytes of guinea pig and dog, the effect of RP58866 on I(Kl), I(to), and I(K) were observed by the whole cell voltage-clamp technique. RESULTS: RP58866 decreased I(Kl) in a concentration-dependent manner, with an IC 50 of (3.4 ± 0.8) μmol · L -1 (n = 6) at -100 mV in guinea pig ventricular cells. In dog ventricular myocytes, RP58866 inhibited I(to) with IC 50 of (2.3 ± 0.5) μmol · L -1 at +40 mV. In guinea pig ventricular cells, RP58866 at 100 μmol · L -1 decreased I(K): I(Kstep) by (58 ± 13)% at +40 mV, and I(Ktail) by (86 ± 17)%, respectively. RP58866 inhibited I(Kstep) with an IC 50 of (7.5 ± 0.8) μmol · L -1, and I(Ktail) with an IC 50 of (3.5 ± 0.9) μmol · L -1. The envelope of tail analysis suggested that both I(Kr) and I(Ks) were inhibited. CONCLUSION: RP58866 inhibits I(Kl), I(to), and I(K) in cardiac myocytes with a similar potency, and is not a specific I(Kl) inhibitor.en_US
dc.languageengen_US
dc.relation.ispartofActa Pharmacologica Sinicaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Arrhythmia Agents - Pharmacologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChromans - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart Ventriclesen_US
dc.subject.meshInhibitory Concentration 50en_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardium - Cytologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPiperidines - Pharmacologyen_US
dc.subject.meshPotassium Channels - Drug Effectsen_US
dc.titleEffects of RP58866 on transmembrane K + currents in mammalian ventricular myocytesen_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.pmid11270975-
dc.identifier.scopuseid_2-s2.0-0032762935en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032762935&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume20en_US
dc.identifier.issue11en_US
dc.identifier.spage961en_US
dc.identifier.epage969en_US
dc.identifier.scopusauthoridYang, BF=7404472748en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridXu, CQ=35228314300en_US
dc.identifier.scopusauthoridNattel, S=36048738800en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats