Acetylcholine activation of single muscarinic K+ channels in isolated pacemaker 
cells of the mammalian heart

Sakmann, Bert; Noma, A.; Trautwein, W.

doi:10.1038/303250a0

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Acetylcholine activation of single muscarinic K+ channels in isolated pacemaker cells of the mammalian heart

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Sakmann, Bert
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Sakmann, B., Noma, A., & Trautwein, W. (1983). Acetylcholine activation of single muscarinic K+ channels in isolated pacemaker cells of the mammalian heart. Nature, 303(5914), 327-808. doi:10.1038/303250a0.

Cite as: https://hdl.handle.net/21.11116/0000-0000-D87E-0

Abstract

Acetylcholine (ACh) released on vagal stimulation reduces the heart rate by increasing K+ conductance of pacemaker cells in the sinoatrial (S-A) node. 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). On the other hand, it has been suggested that m-AChRs may simply regulate the current flow through inward rectifying resting K+ channels (gk1). 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.