Beta-receptor activation increases sodium current in guinea pig heart
Beta-receptor activation increases sodium current in guinea pig heart
复制标题
DOI：
10.1038/aps.2009.96
复制
发表时间：
2009-08-01
影响因子：
8.2
通讯作者：
Li, Ci-zhen
中科院分区：
文献类型：
--
作者：
Wang, Hong-wei;Yang, Zhi-fang;Li, Ci-zhen
目的：研究β受体激活对钠通道电流的影响，以及钠通道电流增加在交感神经兴奋引起心输出量增加中的生理意义。多种实验方法，包括心电图、传统微电极动作电位记录、全细胞电流测量、单通道记录和泵力测量，结果：异丙肾上腺素能剂量依赖性地缩短QRS波，增加动作电位的振幅和最大波幅，增加快钠电流，增加钠通道长开放和爆发模式的出现频率和开放时间常数。膜渗透性cAMP水平的增加具有类似的作用。结论：β-肾上腺素能调节通过改变钠通道模式，增加内向钠电流，加快心室内传导速度，这可能既有利于心脏的同步收缩，又增强其泵血功能。
Aim: To study the influence of beta-receptor activation on sodium channel current and the physiological significance of increased sodium current with regard to the increased cardiac output caused by sympathetic excitation.Methods: Multiple experimental approaches, including ECG, action potential recording with conventional microelectrodes, whole-cell current measurements, single-channel recordings, and pumping-force measurements, were applied to guinea pig hearts and isolated ventricular myocytes.Results: Isoprenaline was found to dose-dependently shorten QRS waves, increase the amplitude and the V-max of action potentials, augment the fast sodium current, and increase the occurrence frequencies and open time constants of the long-open and burst modes of the sodium channel. Increased levels of membrane-permeable cAMP have similar effects. In the presence of a calcium channel blocker, TTX reversed the increased pumping force produced by isoprenaline.Conclusion: Beta-adrenergic modulation increases the inward sodium current and accelerates the conduction velocity within the ventricles by changing the sodium channel modes, which might both be conducive to the synchronous contraction of the heart and enhance its pumping function.