Figure 3.

Coexpression of Cx30 inhibits αβγENaC currents in a dose-dependent manner.A, representative whole-cell current traces recorded in a human αβγENaC-expressing control oocyte or in oocytes injected with both αβγENaC and different amounts of human Cx30 cRNA (1–4 ng/oocyte). Application of amiloride (Ami, 2 μM) and removal of divalent cations from the bath solution for 60 s (Ca²⁺Mg²⁺- Removal) are indicated by corresponding filled and open bars, respectively. Dashed lines indicate zero current level. B, ΔI_{Ca²⁺Mg²⁺-Removal} values were obtained from similar experiments as shown in A and calculated as described in Figure 1. Mean ± SEM and individual data points for each experiment are shown (n = 20, N = 5). C, ENaC-mediated amiloride-sensitive current values (ΔI_Ami) were calculated from similar experiments as shown in A by subtracting the baseline current in the presence of amiloride from the current level reached after amiloride washout. Mean ± SEM and data points for individual oocytes are shown; (n = 68, N = 5). D, the relative inhibitory effect of Cx30 on ENaC was calculated according to the following equation: $\left(\frac{\Delta I_{Ami}}{\Delta I_{Ami}(mean,control)}-1\right)\times 100\%,$ where $\Delta I_{Ami}$ is the amiloride sensitive current of an individual oocyte coexpressing Cx30 and ENaC, whereas $\Delta I_{Ami}(mean,control)$ is the mean $\Delta I_{Ami}$ measured in control oocytes from the same batch but expressing ENaC alone (control). Original data are the same as in C. Mean ± SEM and data points for individual oocytes are shown; ∗∗p < 0.01; ∗∗∗p < 0.001; n.s., not significant; compared with control (markers above the columns) or to another comparison group as indicated; Kruskall–Wallis with Dunn’s post hoc test.