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本文用细胞内微电极技术观察了ＥＴ－１对家兔窦房结起搏细胞电生理活动的影响。所得结果如下：（１）在以ＥＴ－１作表面灌流时，起搏细胞的４相自动去极化的速度（ＶＤＤ）显著减慢，且呈浓度依赖性，结果导致起搏细胞的自发放电频率（ＲＰＦ）降低。（２）由ＥＴ－１引起的ＶＤＤ和ＲＰＦ下降，可由事先投用ＥＴ＿Ａ＾受体选择性阻断剂ＢＱ－１２３（２０，１００μｇ／Ｌ）所阻断。这一结果有力提示，ＥＴ－１对起搏细胞的电生理效应是由ＥＴ＿Ａ受体亚型介导的。（３）事先投用Ｋ＿（ＡＴＰ）通道阻断剂格列苯脲（１０μｍｏｌ／Ｌ），可完全消除ＥＴ－１对起搏细胞的负性频率作用。根据上述结果，似可认为，ＥＴ－１与ＥＴ＿Ａ受体的结合可激活Ｋ＿（ＡＴＰ）通道，致使Ｋ￣＋电流增加和起搏细胞的ＶＤＤ减慢。
In this paper, intracellular microelectrode technique was used to observe the effect of ET-1 on electrophysiological activity of pacemaker cells in sinoatrial node of rabbits. The results obtained are as follows: (1) In the case of surface perfusion with ET-1, the spontaneous polarization of pacephable cells (4) in spontaneous polarization (VDD) slowed significantly and in a concentration-dependent manner, resulting in spontaneous discharge of paced cells The frequency (RPF) decreases. (2) The decrease of VDD and RPF caused by ET-1 can be blocked by pretreatment with ET-A receptor selective blocker BQ-123 (20,100μg / L). This result strongly suggests that the electrophysiological effect of ET-1 on pacemaker cells is mediated by the ET_A receptor subtype. (3) The K (ATP) channel blocker glibenclamide (10μmol / L) was administered beforehand to completely eliminate the negative effect of ET-1 on pacemaker cells. Based on the above results, it is thought that the combination of ET-1 and ET-A receptors activates K-ATP channels, resulting in an increase in K + current and a decrease in VDD of paced cells.