Arrhythmogenesis Toxicity of Aconitine Is Related to Intracellular Ca2+ Signals

Aconitine is a well-known arrhythmogenic toxin and induces triggered activities through cardiac voltage-gated Na + channels. However, the effects of aconitine on intracellular Ca 2+ signals were previously unknown. We investigated the effects of aconitine on intracellular Ca 2+ signals in rat ventri...

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Published in:International journal of medical sciences 2013-08, Vol.10 (9), p.1242-1249
Main Authors: Zhou, Yu-hong, Piao, Xian-mei, Liu, Xue, Liang, Hai-hai, Wang, Lei-min, Xiong, Xue-hui, Wang, Lu, Lu, Yan-jie, Shan, Hong-li
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Language:English
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Summary:Aconitine is a well-known arrhythmogenic toxin and induces triggered activities through cardiac voltage-gated Na + channels. However, the effects of aconitine on intracellular Ca 2+ signals were previously unknown. We investigated the effects of aconitine on intracellular Ca 2+ signals in rat ventricular myocytes and explored the possible mechanism of arrhythmogenic toxicity induced by aconitine. Ca 2+ signals were evaluated by measuring L-type Ca 2+ currents, caffeine-induced Ca 2+ release and the expression of NCX and SERCA2a. Action potential and triggered activities were recorded by whole-cell patch-clamp techniques. In rat ventricular myocytes, the action potential duration was significantly prolonged by 1 µM aconitine. At higher concentrations (5 µM and 10 µM), aconitine induced triggered activities and delayed after-depolarizations (6 of 8 cases), which were inhibited by verapamil. Aconitine (1 µM) significantly increased the I Ca-L density from 12.77 ± 3.12 pA/pF to 18.98 ± 3.89 pA/pF (n=10, p
ISSN:1449-1907
DOI:10.7150/ijms.6541