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. 2019 Mar 27;176(8):1090–1105. doi: 10.1111/bph.14577

Figure 6.

Figure 6

Effects of hesperetin (HSP) on voltage‐dependent kinetics of I Na in the wild‐type (WT) and R1623Q mutants. Current–voltage relationships of I Na in (a) WT and (b) R1623Q under control condition and in the presence of hesperetin (100 μmol·L−1). The dots represent the mean ± SEM (n = 13). Hesperetinsignificantly decreased the current compared with control in the range of voltage from −40 to +20 mV in both the WT and R1623Q channels (P < 0.05, paired t test). Availability and activation curves for (c) WT and (d) R1623Q in control and in the presence of hesperetin (100 μmol·L−1). The dots represent the mean ± SEM (n = 13). Hesperetin significantly shifted the availability curve compared with control in both the WT and R1623Q channels (P < 0.05, paired t test). Dot and line graphs showing the changes in (e) V inac and (f) V act induced by hesperetin (100 μmol·L−1) in both WT and R1623Q mutated channels. Note that hesperetin was more effective in shifting to more hyperpolarized potentials the V inac in the mutant R1623Q channel (n = 13, two‐way ANOVA with Tukey's post hoc test). V inac (and s inac) was −74.8 ± 0.3 mV (6.9 ± 0.3 mV) and −80.6 ± 0.4 mV (6.4 ± 0.4 mV) in WT channel and −75.4 ± 0.5 mV (7.5 ± 0.4 mV) and −87.4 ± 0.8 mV (5.6 ± 0.7 mV) in R1623Q channel in control and hesperetin respectively. V act (and s act) were −34.7 ± 0.4 mV (4.6 ± 0.3 mV) and −34.6 ± 0.4 mV (4.3 ± 0.3 mV) in WT channel and −33.9 ± 0.2 mV (5.5 ± 0.2 mV) and −33.5 ± 0.3 mV (5.6 ± 0.2 mV) in R1623Q channel in control and hesperetin respectively