Effects and mechanisms of store-operated calcium channel blockade on hepatic ischemia-reperfusion injury in rats

Figure 4 Store-operated calcium currents in freshly isolated hepatocytes. A: I-V curves of I_SOC induced by 10 μmol/L IP₃ and 10 mmol/L ethylene glycol tetraacetic acid (EGTA) in hepatocytes, recorded with the voltage ramps from -100 mV to +100 mV, showing the beginning of whole-cell patch-clamp recording (red) and reaching peak current (green) (n = 14); B: Time course of I_SOC development, taken at holding potentials of -100 mV and +100 mV for inward and outward currents, respectively; C: I-V curves of I_SOC obtained by subtraction of baseline from peak current (the red and green sections of the trace, respectively, as described in A), at the time marked “▲” in B; D: Currents induced by 10 mmol/L EGTA following replacement of Ca²⁺ with Ba²⁺ in the external solution (n = 6); E: I-V curves at the three time points indicated by the arrows in panel D: 1, SOC was fully activated by 10 mmol/L EGTA in the pipette solution, 2, 3, The amplitude of I_SOC at -100 mV as a function of time when the external solution was replaced by a solution containing 100 mmol/L Ba²⁺ and no Ca²⁺ or Mg²⁺ for the period indicated in D (n = 6); F: Currents stimulated by 10 mmol/L EGTA. The green trace shows the instantaneous current density-voltage relationship in the range of -100 mV to +100 mV obtained in response to a voltage ramp at the time when inward current was fully developed. The black trace was obtained in response to the presence of 100 μmol/L 2-APB (n = 6); G: Effect of 10 μmol/L A9C on current induced by 10 mmol/L EGTA. The green trace shows the instantaneous current density-voltage relationship in the range of -100 mV to 100 mV obtained in response to a voltage ramp at the time when inward current is fully developed. The black trace was obtained in the presence of 10 μmol/L A9C (n = 5).