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用细胞内微电极技术研究了ＡＴＰ－敏感性钾（Ｋ_（ＡＴＰ））通道和内皮素（ｅｎｄｏｔｈｅｌｉｎ，ＥＴ）在缺氧所致窦房结起搏细胞负性频率中的作用，主要结果如下：（１）缺氧引起窦房结起搏细胞的ＲＰＦ降低和ＡＰＤ缩短，这一效应随时间延长而加重。（２）Ｋ_（ＡＴＰ）通道开放剂ｃｒｏｍａｋａｌｉｍ浓度依赖性地对窦房结起搏细胞有负性频率作用，且明显缩短ＡＰＤ_（５０）。该通道的阻断剂格列苯脲能部分阻断缺氧对起搏细胞的上述效应，表明缺氧效应中有Ｋ_（ＡＴＰ）通道的参与。（３）ＥＴ－１可显著加重缺氧所致的ＲＰＦ降低，使起搏细胞停跳时间前移；而以ＥＴ_Ａ受体阻断剂ＢＱ－１２３预处理窦房结标本后，则能有效地缓解缺氧对起搏细胞的效应，提示内源性ＥＴ－１的释放在缺氧效应中的作用。上述结果表明，缺氧所致起搏细胞的负性频率作用和ＡＰＤ缩短，与Ｋ_（ＡＴＰ）通道的激活和内源性ＥＴ－１的释放有关。
The effect of ATP-sensitive potassium channel (K_ (ATP)) and endothelin (ET) on the negative frequency of pacemaker cells caused by hypoxia was studied by intracellular microelectrode technique. The main results are as follows: (1) Hypoxia caused a decrease of RPF and shortening of APD in pacemaker cells of sinoatrial node. This effect aggravated with time. (2) K (ATP) channel opener cromakalim negatively affected the pacemaker cells of sinoatrial node in a concentration-dependent manner, and significantly shortened APD_ (50). Glibenclamide, a blocker of this channel, partially blocked the above effect of hypoxia on pacemaker cells, indicating the involvement of K (ATP) channels in hypoxia. (3) ET-1 significantly increased the hypoxia-induced decrease of RPF and delayed the pacemaker cell arrest time. However, pretreatment with ET-A receptor antagonist BQ-123 could effectively Alleviate the effect of hypoxia on pacemaker cells, suggesting the role of endogenous ET-1 release in hypoxia. The above results indicate that hypoxia-induced negative effects of pacemaker cells and APD shortening are related to the activation of K-ATP channel and the release of endogenous ET-1.