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. Author manuscript; available in PMC: 2019 Sep 1.
Published in final edited form as: J Cell Physiol. 2018 Mar 25;233(9):7217–7225. doi: 10.1002/jcp.26552

FIGURE 5.

FIGURE 5

AT1aR deletion impairs regulation of ENaC activity by mineralocorticoid receptor (MR) signaling. (a) Summary graph of averaged total ENaC activity, fNPo in Wild type and AT1aR −/− mice in the control and after systemic Deoxycorticosterone acetate (DOCA) injections for 3 consecutive days to maximally stimulate MR. *significant increase versus Wild type control; **significant decrease versus Wild type + DOCA. (b) Summary graph comparing averaged total ENaC activity, fNPo in AT1aR −/− mice kept on low (<0.01% Na+) and control (0.32% Na+) salt intake in the absence (light gray) and presence (dark grey) of concomitant treatment with MR antagonist spironolactone (30 mg/kgBW) in drinking water, respectively. *significant decrease versus AT1aR −/− low salt