| Autor: |
Shi-Sheng Zhou, Yang, Jun, Yao-Qin Li, Lin-Yan Zhao, Ming Xu, Yan-Feng Ding |
| Předmět: |
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| Zdroj: |
Experimental Physiology; Nov2005, Vol. 90 Issue 6, p865-872, 8p, 1 Diagram, 3 Graphs |
| Abstrakt: |
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 ( INa) and action potential (AP), respectively, in single rat cardiac ventricular myocytes. Addition of the Na+ channel agonist aconitine (0.1 μ m) 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 μ m, respectively, without significantly affecting the resting potential of rat ventricular myocytes. Both Cl− channel blockers inhibited INa and induced a leftward shift of the steady-state inactivation of INa. 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 INa. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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