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This Article Full Text Full Text (PDF) All Versions of this Article: 90/6/865    most recent expphysiol.2005.031484v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zhou, S.-S. Articles by Ding, Y.-F. Search for Related Content PubMed PubMed Citation Articles by Zhou, S.-S. Articles by Ding, Y.-F. Related Collections Heart/Cardiac Muscle

¹ Institute of Basic Medical Sciences, Medical College, Dalian University, Dalian 116622, China ² Department of Physiology, Fourth Military Medical University, Xi'an 710032, China ³ Department of Physiology, Xinxiang Medical College, Xinxiang 453003, China

The effects of Cl^– channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid (NFA) on aconitine-induced arrhythmias were investigated. Left ventricular pressure and electrocardiogram were monitored in Langendorff-perfused rat hearts. Whole-cell patch-clamp and current-clamp techniques were used to measure sodium current (I_Na) and action potential (AP), respectively, in single rat cardiac ventricular myocytes. Addition of the Na⁺ channel agonist aconitine (0.1 µM) to the perfusion solution produced polymorphic ventricular arrhythmias with a latent period of 25.5 ± 6.3 s. NPPB could reverse aconitine-induced arrhythmias. A similar effect was observed by using NFA. NPPB and NFA reversibly depressed the upstroke of the AP in a dose-dependent manner with IC₅₀ values of 12.3 and 73.1 µM, respectively, without significantly affecting the resting potential of rat ventricular myocytes. Both Cl^– channel blockers inhibited I_Na and induced a leftward shift of the steady-state inactivation of I_Na. In conclusion, the results of this study demonstrate that NPPB as well as NFA can suppress aconitine-induced arrhythmias in rat hearts mainly by inhibiting cardiac I_Na.

(Received 5 July 2005; accepted after revision 16 August 2005; first published online 23 August 2005)
Corresponding author S.-S. Zhou: Institute of Basic Medical Sciences, Medical College, Dalian University, Dalian 116622, China. Email: zhouss{at}dlu.edu.cn

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