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. Author manuscript; available in PMC: 2023 Jun 1.
Published in final edited form as: Hypertension. 2022 Apr 18;79(6):1227–1236. doi: 10.1161/HYPERTENSIONAHA.121.18734

Figure 6. AT1aR activation on CD11c+ cells attenuates renal sodium retention during hypertension.

Figure 6.

(A) Urinary sodium excretion at baseline and during Ang II infusion. N=6 mice/group. (B) mRNA levels for α-ENaC, β-ENaC, γ-ENaC, NHE3, and NKCC2 in the kidney after 4 weeks of Ang II. (C) kidney protein levels of the sodium transporters as determined by immunoblotting. (D) Densitometry of these blots. normalized to GAPDH. N≥15 mice/group. Data are mean ± SE. “KO” is DC AT1aR KO. Urinary sodium excretion is reported as Na+ (millmoles/ 20gm body weight). “f-y-ENaC” stands for full-length γ-ENaC.