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Low K⁺-induced hyperpolarizations trigger transient depolarizations and action potentials in rabbit ventricular myocytes

M. Akuzawa-Tateyama, M. Tateyama and R. Ochi

The effects of large reductions of [K⁺]_o on membrane potential were studied in isolated rabbit ventricular myocytes using the whole-cell patch clamp technique.

Decreasing [K⁺]_o from the normal level of 5·4 mM to 0·1 mM increased resting membrane potential (V_rest) from -75·6 ± 0·3 to -140·3 ± 1·9 mV (means ± s.e.m; n = 127), induced irregular, transient depolarizations with mean maximal amplitudes of 19·5 ± 1·5 mV and elicited action potentials in 56·7 % of trials. The action potentials exhibited overshoots of 37·9 ± 1·5 mV (n = 72) and sustained plateaux.

Addition of 0·1 mM La³⁺ in the presence of 0·1 mM [K⁺]_o significantly increased V_rest but decreased the amplitude of transient depolarizations and suppressed the firing of action potentials.

Replacement of external Na⁺ or Cl^- with N-methyl-D-glucamine or aspartate, respectively, or internal dialysis with 10 mM EGTA or BAPTA had little effect on low [K⁺]_o-induced membrane potential changes.

Hyperpolarizing voltage clamp pulses to potentials between -110 and -200 mV activated irregular inward currents that increased in amplitude and frequency with increasing hyperpolarization and were depressed by 0·1 mM La³⁺.

The generation of transient depolarizations by low [K⁺]_o can be explained as being a consequence of decreasing the inward rectifier K⁺ current (I_K1) and the appearance of inward currents reflecting electroporation resulting from strong electric fields across the membrane.

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