Wang Wen-Wei, Zhu Yi-Chun, Yao Tai, Zheng Ping, Gong Qian-Ling
Department of Physiology, Medical Center of Fudan University, Shanghai 200032.
Sheng Li Xue Bao. 2002 Apr 25;54(2):149-53.
The experiments were carried out on guinea pig isolated ventricular myocytes by using whole-cell patch clamp. The effects of angiotensin II (Ang II) on potassium ion channels of acute ischemic myocytes were observed. Whole-cell patch clamp recordings showed that physiological potassium current, including delayed rectifier potassium current and inward rectifier potassium current were inhibited under the condition of simulated ischemia, and then further inhibited by treatment with Ang II. ATP-sensitive potassium currents were increased under simulated ischemia and were further enhanced by Ang II treatment.
实验采用全细胞膜片钳技术在豚鼠离体心室肌细胞上进行。观察了血管紧张素II（Ang II）对急性缺血心肌细胞钾离子通道的影响。全细胞膜片钳记录显示，在模拟缺血条件下，包括延迟整流钾电流和内向整流钾电流在内的生理性钾电流受到抑制，随后经Ang II处理后进一步受到抑制。在模拟缺血时ATP敏感性钾电流增加，经Ang II处理后进一步增强。
