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Am J Physiol Heart Circ Physiol (May 2, 2002). doi:10.1152/ajpheart.00721.2001
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Articles in PresS, published online ahead of print May 2, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00721.2001
Submitted on August 13, 2001
Accepted on April 15, 2002

Rate-Dependent [K+]o Accumulation in Canine Right Atria In Vivo: Electrophysiological Consequences

Akira Miyata1, Joshua D Dowell1, Douglas P Zipes1, and Michael Rubart1*

1 Medicine, Krannert Institute of Cardiology, Indianapolis, IN, USA

* To whom correspondence should be addressed. E-mail: mrubartv{at}iupui.edu.

Sudden increases in heart rate cause accumulation of potassium ions in the extracellular space. However, the exact relationship between rate and extracellular potassium concentration ([K+]o)in vivo is unknown. We measured [K+]o in right atria of anesthetized dogs using K+-sensitive electrodes. Peak increase in [K+]o ranged from 0.18±0.04 mmol/L (mean±SEM; cycle length (CL)=350 ms) to 0.80±0.09 mmol/L (CL=250 ms) above baseline (3.50±0.08 mmol/L at CL=380 ms; n=5). During rapid pacing-induced atrial fibrillation, peak increase in [K+]o averaged 0.80±0.07 mmol/L (n=5). Whole-cell current-clamp measurements in single right atrial myocytes (n=5) showed that increases of [K+]o from 3 to 5 mmol/L in 1-mmol/L steps progressively depolarized resting membrane potential and reduced both phase-0 action potential amplitude and maximal upstroke velocity concentration-dependently. 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 extracellular K+ accumulation in vivo is of sufficient magnitude to modulate those cellular electrophysiological properties that determine atrial CVL.




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