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. 2017 Jun 13;175(8):1318–1328. doi: 10.1111/bph.13853

Figure 6.

Figure 6

Exogenous NO reverses the ox‐LDL‐induced increase in ENaC activity via sGC/PKG. (A–C) Representative ENaC single‐channel currents recorded in endothelial cells (left) and summarized ENaC P O (right); basal ENaC activity in the same patch served as its own control (Ctrl). (A) SNP (an NO donor; 1 mM) reversed the increased ENaC activity induced by 10 μg·mL−1 ox‐LDL under Ctrl conditions, no matter whether ox‐LDL was applied to the cell first (upper trace) or SNP was applied to the cell first (lower trace); (B, C) SNP (1 mM) no longer reversed the increased ENaC activity induced by 10 μg·mL−1 ox‐LDL in two separate cells; one was pretreated with 10 μM ODQ, an sGC inhibitor (B); the other was pretreated with 10 μM KT5823 (C), no matter whether SNP was applied to the cell first (upper traces in B and C) or ox‐LDL was applied to the cell first (lower traces in B and C). *P < 0.05 vs. either Ctrl or pre‐treament; n = 6 paired experiments.