ACETYLCHOLINE ACTIVATION OF SINGLE MUSCARINIC K+ CHANNELS IN ISOLATED PACEMAKER CELLS OF THE MAMMALIAN HEART
ACETYLCHOLINE ACTIVATION OF SINGLE MUSCARINIC K+ CHANNELS IN ISOLATED PACEMAKER CELLS OF THE MAMMALIAN HEART
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DOI：
10.1038/303250a0
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发表时间：
1983-01-01
期刊：
影响因子：
64.8
通讯作者：
TRAUTWEIN, W
中科院分区：
文献类型：
--
作者：
SAKMANN, B;NOMA, A;TRAUTWEIN, W
迷走神经刺激时释放的乙酰胆碱（ACh） 1通过增加窦房（S-A）节点起搏器细胞的K+电导来降低心率2,3。起搏器组织中乙酰胆碱激活电流的波动分析表明，这是由于毒蕈碱乙酰胆碱受体（m-AChRs）门控的另一类K+通道打开所致4。另一方面，有人认为m- achr可能只是通过向内整流的静息K+通道（gK1）调节电流5,6。我们在此报道了在兔心脏房室（A-V）和S-A结离体细胞中测定ach激活的单通道K+电流和静息K+通道电流。结果表明，结细胞乙酰胆碱依赖性的K+电导增加是由K+通道介导的，而K+通道与心房细胞和心室细胞的静息K+通道在门控和电导特性上有所不同。然而，结细胞中静止的K+通道与ACh激活的通道相似。
Acetylcholine (ACh) released on vagal stimulation1reduces the heart rate by increasing K+conductance of pacemaker cells in the sinoatrial (S-A) node2,3. Fluctuation analysis of ACh-activated currents in pacemaker tissue showed this to be due to opening of a separate class of K+channels gated by muscarinic ACh receptors (m-AChRs)4. On the other hand, it has been suggested that m-AChRs may simply regulate the current flow through inward rectifying resting K+channels (gK1)5,6. We report here the measurement of ACh-activated single channel K+currents and of resting K+channel currents in isolated cells of the atrioventricular (A-V) and S-A node of rabbit heart. The results show that the ACh-dependent K+conductance increase in nodal cells is mediated by K+channels which are different in their gating and conductance properties from the inward rectifying resting K+channels in atrial and ventricular cells. The resting K+channels in nodal cells are, however, similar to those activated by ACh.