Lee S, Park M, So I, Earm Y E
Department of Physiology and Biophysics, Seoul National University College of Medicine, Korea.
Pflugers Arch. 1994 Jun;427(3-4):378-80. doi: 10.1007/BF00374548.
We have investigated the effect of NADH and NAD on the gating of large conductance Ca(2+)-activated K(KCa) channels in arterial smooth muscle cells isolated from small pulmonary artery (outer diameter < 300 microns) and ear artery, using the patch clamp technique. In the inside-out configuration, intracellularly applied 2 mM NADH inhibited the activity of KCa channels in pulmonary arterial smooth muscle cells, while it had no significant effect on ear arterial smooth muscle cells. On the other hand, 2 mM NAD increased the opening of KCa channels in pulmonary arterial smooth muscle cells. The effects of another intracellular redox couple, glutathione(GSH) and glutathione disulfide(GSSG) were also dependent on their redox potentials. GSH(5 mM) inhibited KCa channels activity, while GSSG(5 mM) increased the activity of pulmonary arterial smooth muscle cells. It could be concluded that the modulation of KCa channels by intracellular redox state contributes, at least in part, to the hypoxic suppression of outward current in pulmonary arterial smooth muscle cells.
我们采用膜片钳技术，研究了还原型辅酶Ⅰ（NADH）和辅酶Ⅰ（NAD）对从小肺动脉（外径<300微米）和耳动脉分离的动脉平滑肌细胞中大电导钙激活钾（KCa）通道门控的影响。在膜内面向外模式下，细胞内施加2 mM NADH可抑制肺动脉平滑肌细胞中KCa通道的活性，而对耳动脉平滑肌细胞无显著影响。另一方面，2 mM NAD可增加肺动脉平滑肌细胞中KCa通道的开放。另一细胞内氧化还原对，即谷胱甘肽（GSH）和谷胱甘肽二硫化物（GSSG）的作用也取决于它们的氧化还原电位。5 mM GSH可抑制KCa通道活性，而5 mM GSSG可增加肺动脉平滑肌细胞的活性。可以得出结论，细胞内氧化还原状态对KCa通道的调节至少部分地促成了肺动脉平滑肌细胞外向电流的低氧抑制。
