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. Author manuscript; available in PMC: 2013 Jun 21.
Published in final edited form as: Curr Opin Nephrol Hypertens. 2012 Jan;21(1):52–60. doi: 10.1097/MNH.0b013e32834db4a0

Figure 3. Purinergic inhibition of ENaC allows this channel to respond appropriately to sodium balance.

Figure 3

Single channel current traces of ENaC in cell attached patches on ASDN isolated from mice maintained on a sodium free (A) and a high sodium diet (B) without (top) and with (bottom) addition of suramin plus hexokinase to the bathing solution. Inward current is downward with closed state noted with C. *significant decrease compared to sodium free (<0.01%) condition; **significant increase compared to control. Data originally presented in [9]. C. Summary graph showing the effects on ENaC activity of suramin plus hexokinase (gray bars) as compared to basal activity (black bars) in ASDN from mice fed a sodium free, regular sodium and high sodium diet. *significant increase compared to wild-type under identical feeding conditions. Data originally presented in [9]. D. Summary graph comparing ENaC activity in ASDN from wild-type (black bars) versus P2Y2 receptor knockout (gray bars) mice maintained with sodium free, regular sodium and high sodium diets. Data originally presented in [9]. E. Summary graph showing fractional ENaC activity (activity with high sodium feeding / activity with sodium free feeding) in wild-type (wt) and P2Y2 receptor and Cx30 knockout mice in the absence (gray circles) and presence (black circles) supplementing with DOCA. Activity calculated as fNPo where f is the frequency of observing at least one active ENaC in a patch, N is the mean number of ENaC per patch that contained active channels, and Po is open probability. Data originally presented in [10] and [22].