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

1. 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. 2. Decreasing [K+]o from the normal level of 5.4 mM to 0.1 mM increased resting membrane potential (Vrest) 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. 3. Addition of 0.1 mM La3+ in the presence of 0.1 mM [K+]o significantly increased Vrest but decreased the amplitude of transient depolarizations and suppressed the firing of action potentials. 4. 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. 5. 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+. 6. The generation of transient depolarizations by low [K+]o can be explained as being a consequence of decreasing the inward rectifier K+ current (IK1) and the appearance of inward currents reflecting electroporation resulting from strong electric fields across the membrane.