Rate-dependent [K+](o) accumulation in canine right atria in vivo: electrophysiological consequences.
Sudden increases in heart rate cause accumulation of K+ in the extracellular space. However, the exact relationship between rate and extracellular K+ concentration ([K+](o)) in vivo is unknown. We measured [K+](o) in right atria of anesthetized dogs by using K(+)-sensitive electrodes. Peak increase in [K+](o) ranged from 0.18 +/- 0.04 mM [means +/- SE; cycle length (CL) = 350 ms] to 0.80 +/- 0.09 mM (CL = 250 ms) above baseline (3.50 +/- 0.08 mM at CL = 380 ms; n = 5). During rapid pacing-induced atrial fibrillation, peak increase in [K+](o) averaged 0.80 +/- 0.07 mM (n = 5). Whole cell current-clamp measurements in single right atrial myocytes (n = 5) showed that raising [K+](o) from 3 to 5 mM in 1-mM steps progressively depolarized resting membrane potential and reduced both phase 0 action potential amplitude and maximal upstroke velocity. Multisite epicardial mapping (n = 4) demonstrated that sudden rate increases changed longitudinal conduction velocity (CV(L)) by -3.6 +/- 1.8% to -5.9 +/- 1.2% over a CL range of 330 to 250 ms. Our observations suggest that rate-related [K+](o) accumulation in vivo is of sufficient magnitude to modulate those cellular electrophysiological properties that determine atrial CV(L).
Krannert Institute of Cardiology, Indianapolis, IN 46202, USA.
Akira
A
Miyata
Joshua D
JD
Dowell
Douglas P
DP
Zipes
Michael
M
Rubart
D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology / Q000378:metabolism; D016280:Atrial Function, Right; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004594:Electrophysiology; D006329:Heart Conduction System / Q000502:physiology; D006339:Heart Rate / Q000502:physiology*; D008564:Membrane Potentials; D009206:Myocardium / Q000378:metabolism*; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism*; D013997:Time Factors
D011188:Potassium