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Role of M3 receptor in aconitine/barium-chloride-induced preconditioning against arrhythmias in rats

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Abstract

We demonstrated here that an initial treatment with aconitine- or barium-chloride-induced arrhythmias and resulted in reduced susceptibility of the heart to the induction of arrhythmias by a repeated drug treatment 24 h after the initial one, a delayed preconditioning cardioprotection. This delayed preconditioning was accompanied by enhanced expression of cardiac muscarinic M3 receptor and abolished by M3-selective antagonist. We conclude that muscarinic M3 receptors might play an important role in conferring the pharmacological preconditioning against arrhythmias. This study thus expands our understanding of the cellular function and pathophysiological roles of muscarinic M3 receptor and reconsolidates our view of cardioprotective effects of muscarinic M3 receptor on myocardium.

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Acknowledgments

This work was supported by the National Natural Science Foundation of China (30672462) Specialized Research Fund for the Doctoral Program of Higher Education (20060226019, 20050226010), and the Heilongjiang Postdoctoral Sustentation Fund, China. Innovation Fund for Graduate student of Harbin Medical University, China (HCXS2006001).

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Correspondence to Yan-jie Lu or Bao-feng Yang.

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Yan Liu and Juan Du made equal contribution to this study.

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Liu, Y., Du, J., Gao, Y. et al. Role of M3 receptor in aconitine/barium-chloride-induced preconditioning against arrhythmias in rats. Naunyn-Schmied Arch Pharmacol 379, 511–515 (2009). https://doi.org/10.1007/s00210-008-0376-6

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  • DOI: https://doi.org/10.1007/s00210-008-0376-6

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