Acetylcholine activation of single muscarinic K+ channels in isolated pacemaker cells of the mammalian heart.
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.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D001283:Atrioventricular Node / Q000502:physiology*; D004553:Electric Conductivity; D006329:Heart Conduction System / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology*; D011188:Potassium / Q000502:physiology; D011817:Rabbits; D011950:Receptors, Cholinergic / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000502:physiology*; D012849:Sinoatrial Node / Q000502:physiology*
D007473:Ion Channels; D011950:Receptors, Cholinergic; D011976:Receptors, Muscarinic; D000109:Acetylcholine; D011188:Potassium