Roles of stretch-activated channels and NADPH oxidase 2 in the induction of twitch contraction by muscle stretching in rat ventricular muscle
Roles of stretch-activated channels and NADPH oxidase 2 in the induction of twitch contraction by muscle stretching in rat ventricular muscle
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DOI：
10.1007/s00424-021-02657-5
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发表时间：
2022-01-23
影响因子：
4.5
通讯作者：
Miura，Masahito
中科院分区：
文献类型：
--
作者：
Sato，Haruka;Nagano，Tsuyoshi;Miura，Masahito
机电反馈意味着肌肉拉伸导致膜电位去极化。我们研究了肌肉拉伸是否会以肌节长度 (SL) 阈值诱导动作电位和抽搐收缩，以及拉伸激活通道 (SAC) 和拉伸激活 NADPH 氧化酶（X-ROS 信号传导）在诱导过程中发挥的作用。小梁取自大鼠心脏的右心室。测量了力、SL 和 [Ca2+]。在电气列车最后一次刺激后 0.5 秒，从 2.0 μm 的 SL 开始进行不同程度的拉伸，间隔为 0.4 秒，持续 7.5 秒。 SL 抽搐定义为拉伸引起抽搐收缩的最小 SL。肌肉拉伸诱导抽搐收缩，阈值为 SL，刺激间隔为 0.4 秒 ([Ca2+]o= 0.7 mmol/L)。增加刺激间隔和 [Ca2+]o 以及添加 1 μmol/L 异丙肾上腺素不会改变 SLtwitch。添加10 μmol/L Gd3+、100 μmol/L或200 μmol/L链霉素和5 μmol/L GsMTx4不会改变SLtwitch。添加1 μmol/L兰尼碱和3 μmol/L二亚苯基碘鎓氯化物后，SLtwitch没有变化。相比之下，通过将细胞外 K+ 从 5 mmol/L 提高到 10 mmol/L 并在膜电位不应期增加拉伸，可以增加 SLtwitch。拉伸引起的抽搐收缩更频繁地引起心律失常。这些结果表明，肌肉拉伸可以在 SL 阈值下诱导抽搐收缩，并与心律失常的发生有关，而 SAC 和 X-ROS 信号传导在诱导过程中不起作用。
Mechano-electric feedback means that muscle stretching causes depolarization of membrane potential. We investigated whether muscle stretching induces action potential and twitch contraction with a threshold of sarcomere length (SL) and what roles stretch-activated channels (SACs) and stretch-activated NADPH oxidase (X-ROS signaling) play in the induction. Trabeculae were obtained from the right ventricles of rat hearts. Force, SL, and [Ca2+]iwere measured. Various degrees of stretching from the SL of 2.0 μm were applied 0.5 s after the last stimulus of the electrical train with 0.4-s intervals for 7.5 s. The SLtwitchwas defined as the minimal SL at which twitch contraction was induced by the stretching. Muscle stretching induced twitch contraction with a threshold of SL at 0.4-s stimulus intervals ([Ca2+]o= 0.7 mmol/L). The SLtwitchwas not changed by increasing the stimulus intervals and [Ca2+]oand by adding 1 μmol/L isoproterenol. The SLtwitchwas not changed by adding 10 μmol/L Gd3+, 100 μmol/L or 200 μmol/L streptomycin, and 5 μmol/L GsMTx4. The SLtwitchwas not changed by adding 1 μmol/L ryanodine and 3 μmol/L diphenyleneiodonium chloride. In contrast, the SLtwitchwas increased by elevating extracellular K+from 5 to 10 mmol/L and by adding the stretching during the refractory period of membrane potential. The addition of the stretching-induced twitch contraction more frequently induced arrhythmias. These results suggest that muscle stretching can induce twitch contraction with a threshold of SL and concern the occurrence of arrhythmias and that SACs and X-ROS signaling play no roles in the induction.