Change in late sodium current of atrial myocytes in spontaneously hypertensive rats with allocryptopine treatment

被引:7
|
作者
Dong, Ying [1 ]
Huang, Yun [2 ]
Wu, Hong-lin [1 ]
Ke, Jun [3 ]
Yin, Yuan-li [1 ]
Zhu, Chao [1 ]
Li, Bin [1 ]
Li, Jie [1 ]
Gao, Lei [1 ]
Xue, Qiao [1 ]
Zhang, Jian-cheng [3 ]
Li, Yang [1 ]
机构
[1] Chinese Peoples Liberat Army Gen Hosp, Dept Cardiol, Beijing 100853, Peoples R China
[2] Huazhong Univ Sci & Technol, Dept Gerontol, Union Hosp, Tongji Med Coll, Wuhan 430022, Hubei, Peoples R China
[3] Fujian Med Univ, Prov Clin Med Coll, Fuzhou 350001, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
allocryptopine; spontaneously hypertensive rats; atrial myocytes; late sodium current; STRESS KINASE JNK; INCREASED SUSCEPTIBILITY; ALPHA-ALLOCRYPTOPINE; ACTION-POTENTIALS; FIBRILLATION; INHIBITION; RANOLAZINE; MUTATION; ONSET;
D O I
10.5830/CVJA-2018-072
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aim: We aimed to study the effect of allocryptopine (All) on the late sodium current (I-Na,I-Late) of atrial myocytes in spontaneously hypertensive rats (SHR). Methods: The enzyme digestion method was used to separate single atrial myocytes from SHR and Wistar-Kyoto (WKY) rats. I-Na,I-Late was recorded using the patch-clamp technique, and the effect of All was evaluated on the current. Results: Compared with WKY rat cells, an increase in the I-Na,I-Late current in SHR myocytes was found. After treatment with 30 mu M All, the current densities were markedly decreased; the ratio of I-Na,I-Late/I-Na,I-peak of SHR was reduced by30 mu M All. All reduced I-Na,I-Late by alleviating inactivation of the channel and increasing the window current of the sodium channel. Furthermore, I-Na,I-Late densities of three SCN5A mutations declined substantially with 30 mu M All in a concentration-dependent manner. Conclusion: The results clearly show that an increase in I-Na,I-Late in SHR atrial myocytes was inhibited by All derived from Chinese herbal medicine.
引用
收藏
页码:79 / 86
页数:8
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