Renal damage inhibited in mice lacking angiotensinogen gene subjected to unilateral ureteral obstruction.

Objectives To determine how angiotensin II (Ang II) contributes to renal interstitial fibrosis, the inflammatory response, and tubular cell apoptosis and proliferation in unilateral ureteral obstruction using mice genetically deficient in angiotensinogen ( Agt −/− ). Methods The left kidney of wild-type mice (WT; C57BL/6) and Agt −/− mice was obstructed for 2 weeks, and then both kidneys were harvested. The serum Ang II levels were determined by radioimmunoassay. The expression of transforming growth factor-β in renal tissue was assessed using enzyme-linked immunosorbent assay. The renal tissue was stained with Masson's trichrome. Renal tubular proliferation and apoptosis was detected by immunostaining for proliferating cell nuclear antigen and single-stranded DNA, respectively. Interstitial leukocyte and macrophage infiltration was investigated by immunostaining for CD45 and F4/80, respectively. Results The serum Ang II levels in the Agt −/− mice were significantly lower than those in the WT mice ( P Agt −/− mice was significantly lower than that in WT mice ( P Agt −/− obstructed kidneys than in the WT obstructed kidneys ( P Agt −/− obstructed kidneys than in the WT obstructed kidneys ( P P Agt −/− obstructed kidneys than in the WT obstructed kidneys ( P P Conclusions The results of the present study support the targeting of Ang II as a reasonable approach by which to prevent renal tissue damage in unilateral ureteral obstruction.