MUSCARINIC REGULATION OF MEMBRANE ION CHANNELS IN AIRWAY SMOOTH-MUSCLE CELLS
MUSCARINIC REGULATION OF MEMBRANE ION CHANNELS IN AIRWAY SMOOTH-MUSCLE CELLS
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DOI：
10.1016/0006-2952(92)90652-y
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发表时间：
1992-01-09
影响因子：
5.8
通讯作者：
TOMASIC, M
中科院分区：
文献类型：
--
作者：
KOTLIKOFF, MI;KUME, H;TOMASIC, M
我们已经证明，毒蕈碱激动剂刺激气道平滑肌导致两种膜离子通道蛋白的协调调节。 这两个通道以类似的方式调制，尽管它们对开放通道概率的影响相反。 在K（Ca）的情况下，通道活性的电压依赖性向更正的电位移动，而在电压依赖性钙通道的情况下向更负的电位移动。 类似地，K（Ca）通道停留时间动力学向短开放寿命转变，而长开放状态有利于大振幅电压依赖性钙通道。 虽然对钙通道的分子偶联知之甚少，但K（Ca）通道的毒蕈碱抑制是通过百日咳毒素敏感的鸟嘌呤核苷酸结合蛋白介导的。
We have demonstrated that stimulation of airway smooth muscle by muscarinic agonists results in a coordinated modulation of two membrane ion channel proteins. Both channels are modulated in a similar way, although their effects on open-channel probability are opposite. The voltage-dependence of channel activity is shifted to more positive potentials in the case of K(Ca), and to more negative potentials in the case of the voltage-dependent calcium channels. Similarly, K(Ca) channel dwell-time kinetics are shifted to short open lifetimes, whereas the long open state is favored for the large-amplitude voltage-dependent calcium channel. Although little is known about the molecular coupling of calcium channels, muscarinic inhibition of K(Ca) channels is mediated through a pertussis toxin-sensitive guanine nucleotide binding protein.