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Am J Physiol Heart Circ Physiol 283: H506-H517, 2002. First published May 2, 2002; doi:10.1152/ajpheart.00721.2001
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Vol. 283, Issue 2, H506-H517, August 2002

Rate-dependent [K+]o accumulation in canine right atria in vivo: electrophysiological consequences

Akira Miyata, Joshua D. Dowell, Douglas P. Zipes, and Michael Rubart

Krannert Institute of Cardiology, Indianapolis, Indiana 46202

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 (CVL) 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 CVL.

atrium; fibrillation; tachycardia; potassium


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