摘要
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。
The effects of endothelin- 1 (ET- 1 ) on the electrophysiological activity of pacemaker cells of rabbit sino-atrial node were examined by using intracellular microelectrodetechnique. The results obtained were as follows: (1) With super fusion of ET-1 (130 nmol/L), the velocity of diastolic depolarization (VDD) of Pacemaker cells was significantly decreased in a concentration dependent manner, resulting in a reduced rate ofpacemaker firing (RPF). (2) The decreases in RPF and VDD induced by ET-1 couldbe virtually blocked by pretreatment with ET_A receptor blocker BQ-123 (20 or 100 μg/L). It was strongly suggested that the electrophysiological effects of ET-1 on the pacemaker cells were mediated by the ET_A receptor. (3) The negative chronotropic actionof ET-1 on the pacemaker cells was totally abolished by pretreatment with a kind ofK_(ATP) channel blocker glibenclamide (10 μmol/L). On the basis of above results, it appears that the binding of ET-1 with ET_A receptor may induce an activation of K_(ATP) channels with resultant increase in K￣+ current so as to decrease the velocity of diastolic depolarization in the pacemaker cells.
出处
《生理学报》
CAS
CSCD
北大核心
1996年第1期53-58,共6页
Acta Physiologica Sinica
基金
国家自然科学基金
关键词
内皮素
窦房结
心电生理
endothelin
endothelin receptor
sino-atrial node
glibenclamide
BQ-123
electrophysiology
