Figure 2. BNP deletion does not lead to marked renal pathology.

(A) Urine volume, calculated creatinine clearance, and urinary excreted protein at nine months were measured in Nppb−/− (n = 5) and age-matched control Nppb+/+ (n = 5). (B) Representative hematoxylin and eosin stained renal sections of Nppb−/− and Nppb+/+ (Black arrow indicates noticeably enlarged artery present in Nppb−/− section), and (C) quantification of renal pathology in Nppb−/− (n = 5) and Nppb+/+ (n = 4). (D) (Left) Representative microphotographs of immunofluorescent renal sections from 9 month Nppb−/− and 9 month Nppb+/+; anti-Desmin (Desmin, Red), and anti-Podocin (Blue). (Right) Representative Nppb−/− and Nppb+/+ glomeruli immunofluorescent imaging of anti-basic fibroblast growth factor 2 (Fgf2, Red) and anti-podocin (Blue), and nuclear counter stain, DAPI (White). (E) RT-PCR quantification of Collagen type 1a1 (Col1a1), Fibronectin-1 (Fn1), Transforming growth factor-β (TGFβ), Tissue inhibitor metalloprotease-1 (Timp1), Atrial Natriuretic Peptide (Nppa), B-type Natriuretic Peptide (Nppb), Natriuretic Peptide Receptors 1 and 2 (Npr1, Npr2, respectively) and Renal damage associated genes; Apolipoprotein E (Apoe1), Vascular endothelial growth factor (VegF), Jagged1 (Jag1) and Nephrosis 1 (Nphs1) transcripts are corrected to house keeping gene GAPDH. Nppb−/− (n = 6) and age-matched control Nppb+/+ (n = 6). *P < 0.05 vs Nppb+/+ by t test.