FIG 2.

Vav1 gene deficiency protects against AngII-triggered cardiorenal dysfunctions. (A to E) Status of the indicated cardiovascular (A to C) and renal (D and E) parameters in mice of the indicated genotypes infused with AngII (+) or left untreated (−). *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001 (n = 10). a.u., arbitrary units. (F and G) Mean arterial pressure evolution (F) and area under the curve (AUC) (G) for the indicated mouse strains and treatments. *, P ≤ 0.05; ***, P ≤ 0.001 (n = 6). (H) Kinetics of cardiorenal fibrosis development in AngII-treated WT mice. *, P ≤ 0.05 (n = 4). (I and J) Evolution (I) and AUC (J) of mean arterial pressure in mice of the indicated genotypes in the presence or absence of l-NAME. ***, P ≤ 0.001 (n = 4). (K to N) Status of the indicated vascular (K), heart (L and M), and renal (N) parameters in WT and Vav1^−/− mice at the end of l-NAME treatment. Note that, in contrast to AngII infusion, oral administration of l-NAME does not induce aorta remodeling even in WT mice (K). *, P ≤ 0.05; ***, P ≤ 0.001 (n = 4). Statistical differences from untreated WT controls or between the indicated experimental groups are indicated.