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Fig. 2 | The Journal of Physiological Sciences

Fig. 2

From: Overexpression of the HCN2 channel increases the arrhythmogenicity induced by hypokalemia

Fig. 2

Hypokalemia-induced spontaneous action potentials (SAPs) in the myocytes of transgenic mice overexpressing the hyperpolarization-activated, cyclic nucleotide-sensitive (HCN) channel in the heart (HCN2-Tg mice). a The perfusion with the 3 mM [K+]o solution is shown by the blue bar. The RMP in the 5.4 mM [K+]o solution was − 81.4 mV. In the 3 mM [K+]o solution, the RMP was hyperpolarized to − 86.0 mV, followed by the generation of SAPs. The red bar indicates the perfusion with 10 μM IVA. After the termination of the SAPs, the RMP was − 90.4 mV. The inset shows the expanded trace of the SAPs. b The incidences of SAPs (black portion of bar) in the 3 mM K+ solution: WT, 0% (0 of 11 cells); HCN2-Tg, 55.0% (11 of 20 cells). Asterisk indicates that difference is statistically significant at p  < 0.01 (χ2 test). c The summary of firing rates (FRs) and maximal diastolic potentials (MDPs) of the SAPs. The gray symbols were obtained in each myocyte by averaging 10 successive SAPs. The red symbol indicates the mean values of the MDP (− 46.6 ± 10.6 mV) and the FR (201.8 ± 82.6 bpm) averaged from 10 myocytes. d The induced AP of HCN2-Tg mouse myocytes in the 5.4 mM [K+]o solution (blue line) and 3 mM [K+]o solution (black line). The RMP and action potential duration at 90% repolarization (APD90) were − 83.8 mV and 31.0 ms, respectively, in the 5.4 mM [K+]o solution and − 88.1 mV and 36.8 ms, respectively, in the 3 mM [K+]o solution. e. The effect of 10 μM IVA on the AP in the 3 mM [K+]o solution. The AP was recorded in the same HCN2-Tg mouse myocytes as those shown in d (the black line, control; the red line, with 10 μM IVA). The application of IVA hyperpolarized the RMP from − 88.1 to − 94.0 mV and shortened the APD90 from 36.8 to 29.8 ms (color figure online)

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