Acetylcholine Activation of Single Muscarinic K+ Channels in Isolated Pacemaker Cells of the Mammalian Heart

Nature. 1983 May 19-25;303(5914):250-3. doi: 10.1038/303250a0.

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.

MeSH terms

  • Acetylcholine / physiology*
  • Animals
  • Atrioventricular Node / physiology*
  • Electric Conductivity
  • Heart Conduction System / physiology*
  • Ion Channels / physiology*
  • Potassium / physiology
  • Rabbits
  • Receptors, Cholinergic / physiology*
  • Receptors, Muscarinic / physiology*
  • Sinoatrial Node / physiology*

Substances

  • Ion Channels
  • Receptors, Cholinergic
  • Receptors, Muscarinic
  • Acetylcholine
  • Potassium