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J Appl Physiol 101: 1170-1176, 2006. First published June 8, 2006; doi:10.1152/japplphysiol.00297.2006
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Slow diffusion of K+ in the T tubules of rat cardiomyocytes

Fredrik Swift,1,2 Tævje A. Strømme,1,2 Bjørn Amundsen,1,2 Ole M. Sejersted,1,2 and Ivar Sjaastad1,2,3

1Institute for Experimental Medical Research, Ullevaal University Hospital; 2Center for Heart Failure Research, University of Oslo; and 3Department of Cardiology, Ullevaal University Hospital, Oslo, Norway

Submitted 10 March 2006 ; accepted in final form 5 June 2006

Cardiomyocyte contractility is regulated by the extracellular K+ concentration ([K+]o). Potassium dynamics in the T tubules during the excitation-contraction cycle depends on the diffusion rate of K+, but this rate is not known. Detubulation of rat cardiomyocytes was induced by osmotic shock using formamide, which separated the surface membrane from the T tubules. Changes in current and membrane potential in voltage-clamped (–80 mV) and current-clamped control and detubulated cardiomyocytes were compared during rapid switches between 5.4 and 8.1 mM [K+]o, and the results were simulated in a mathematical model. In the voltage-clamp experiments, the current changed significantly slower in control than in detubulated cardiomyocytes during the switch from 5.4 to 8.1 mM [K+]o, as indicated by the times to achieve 25, 50, 90, and 95% of the new steady-state current [control (ms) t25 = 98 ± 12, t50 = 206 ± 20, t90 = 570 ± 72, t95 = 666 ± 92; detubulated t25 = 61 ± 11, t50 = 142 ± 17, t90 = 352 ± 52, t95 = 420 ± 69]. These time points were not significantly different either during the 8.1 to 5.4 mM [K+]o switch or in current-clamped cardiomyocytes switching from 5.4 to 8.1 mM [K+]o. Mathematical simulation of the difference current between control and detubulated cardiomyocytes gave a t-tubular diffusion rate for K+ of ~85 µm2/s. We conclude that the diffusion of K+ in the T tubules is so slow that they constitute a functional compartment. This might play a key role in local regulation of the action potential, and thus in the regulation of cardiomyocyte contractility.

mathematical model; detubulation; rapid perfusion; electrophysiology


Address for reprint requests and other correspondence: F. Swift, Institute for Experimental Medical Research, Ullevaal Univ. Hospital, Kirkeveien 166, N-0407 Oslo, Norway (e-mail: fredrik.swift{at}medisin.uio.no)




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