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. 2001 Jun 15;533(Pt 3):697–710. doi: 10.1111/j.1469-7793.2001.t01-1-00697.x

Figure 4. Inward Ba2+ currents in wild-type and Kir2.1−/− neonatal ventricular myocytes.

Figure 4

A and B, Ba2+ currents through T- and L-type Ca2+ channels were recorded in the presence of external TTX and internal Cs+ from voltage-clamped neonatal myocytes isolated from wild-type and Kir2.1−/− mice. For each family of current traces, the voltage was stepped from a holding potential of −80 mV to potentials of −40 to +50 mV (in 15 mV increments). Cell capacitances were 17 and 16 pF, respectively. C, steady state currents (means ±s.e.m.) were plotted as a function of voltage in wild-type (n = 9) and Kir2.1−/− (n = 9) myocytes, with and without the addition of 1 μm nifedipine to reduce L-type currents. Currents were measured 50 ms into the voltage pulse and were normalized to cell capacitance to control for cell surface area.