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. 2016 Jun 22;28(1):209–217. doi: 10.1681/ASN.2016010085

Figure 3.

Figure 3.

NKCC2 and NCC activities and localization in Clcnk2−/− mice. Both furosemide (Furo, A) and hydrochlorothiazide (HCTZ, E) elicit significant natriuresis in Clcnk2+/+ mice 3 hours after intraperitoneal injection. Furosemide induced natriuresis is abolished in Clcnk2−/− mice and HCTZ natriuretic effects strongly blunted. In the renal cortex of Clcnk2+/+ and Clcnk2−/− mice, both NKCC2 (B) and NCC (F) localize to the apical membrane of the TAL and the DCT. In Clcnk2−/− mice, phospho-NKCC2 signals are reduced in some TAL (∞ in C panel) whereas signals in some TAL are normal (star in C panel) as compared with Clcnk2+/+ mice. NCC signals are also reduced. Decreased signal intensity is also observed for phospho-NCC (G). The DCT in Clcnk2−/− mice has abnormal flattened epithelium and dilatation of the lumen. Western blot for NKCC and pNKCC2 (D) and NCC and pNCC (H) on whole kidney lysates from Clcnk2+/+ and Clcnk2−/− mice. Statistical significance was analyzed by unpaired t test (D, H) or ANOVA with repeated measures (A, E). The effect of the pharmacological treatment reaches significant levels for both HCTZ and furosemide. Bonferroni multiple comparisons are presented in the figure and compare the effect of the treatment for Clcnk2+/+ and Clcnk2−/− mice *P<0.05; ****P<0.001. Furo (Clcnk2+/+, n=9; Clcnk2−/−, n=5); HCTZ (Clcnk2+/+, n=10; Clcnk2−/−, n=8). In panels B, C, F, and G, scale bar = 25 µm.