Electrophysiological evidence for a gradient of G protein-gated K+ current in adult mouse atria.
Whole cell current and voltage clamp techniques were used to examine the properties of acetylcholine-sensitive K+ current (IKACh) in myocytes from adult mouse atrium. Superfusion of a maximal dose of carbachol (CCh; 10 microM) caused a substantial increase in K+ current in all myocytes examined. The current-voltage (I-V) relation of maximally activated IKACh exhibited weak inward rectification. Consequently, CCh increased the amount of depolarising current necessary to evoke action potentials (APs), and APs evoked in CCh had significantly shorter durations than control APs (P<0.05). The effects of CCh on K+ current and on AP properties were blocked by the muscarinic receptor antagonist methoctramine (1 microM). ACh (10 microM) activated a K+ current with identical properties to that activated by CCh, as did the A1 receptor agonist adenosine (100 microM). Right atrial myocytes had significantly more IKACh than left atrial myocytes (P<0.05), regardless of whether IKACh was evoked by superfusion of muscarinic or A1 receptor agonists. IKACh current density was significantly higher in SA node myocytes than either right or left atrial myocytes. These data identify a gradient of IKACh current density across the supraventricular structures of mouse heart. This gradient, combined with the heterogeneous distribution of parasympathetic innervation of the atria, may contribute to the proarrhythmic ability of vagal nerve stimulation to augment dispersion of atrial refractoriness.
Lomax
Alan E
AE
Department of Physiology and Biophysics, University of Calgary, Alberta, Canada T2N 4N1.
Rose
Robert A
RA
Giles
Wayne R
WR
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D004594:Electrophysiology; D019204:GTP-Binding Proteins / Q000502:physiology*; D006325:Heart Atria / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*
D015221:Potassium Channels; D019204:GTP-Binding Proteins; D000241:Adenosine