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. 2019 Sep;189(9):1721–1731. doi: 10.1016/j.ajpath.2019.05.020

Figure 2.

Figure 2

Lack of Npr2 worsens kidney dysfunction in response to salt. A: Fluid intake for 24 hours across Npr2 mice. B: Urine volume for 24 hours across Npr2 mice. White bars are baseline values. Black bars are values after 2 weeks of intake of 1% NaCl in drinking water. C and D: A ratio of urine albumin/plasma creatinine (C) and plasma cGMP (D) across Npr2 genotypes after 2 weeks of 1% NaCl intake in drinking water. Black bars are Npr2 wild-type (Npr2+/+) mice. Gray bars are Npr2 heterozygous (Npr2+/−) mice. White bars are Npr2 knockout (Npr2−/−) mice. E: Representative ultrasound images of a transverse plane of kidneys across Npr2 mice. Blue outlined areas define kidney boundaries. White arrowheads point to vascularity. F: Kidney volumes based on 3-dimensional (3D) imaging of the kidneys across Npr2 genotypes. G: Percentages of the kidney vasculature based on 3D imaging of the kidneys across Npr2 genotypes. H: Renal artery resistive index based on ultrasound imaging across Npr2 genotypes. White bars are baseline values. Black bars are values after 2 weeks of 1% NaCl intake in drinking water. Data are expressed as means ± SEM. n = 7 to 11 per group (A, B, and F–G); n = 5 to 9 per group (C and D). ∗P < 0.05 versus Npr2+/+ (baseline); †P < 0.05 versus Npr2+/+ (1% NaCl); ‡P < 0.05 versus Npr2−/− (baseline); §P < 0.05 versus Npr2−/− (1% NaCl).