Fig. 8.

Effect of drug treatments on the renin-angiotensin system (RAS) in the kidney. Total RNA or kidney lysates were obtained from nondiabetic mice (C) and diabetic mice treated with V, L, DL, L+DL, or L+DH at week 20. A and B: RT-PCR analysis (A) and quantification (B) of renin mRNA levels in the kidney of all mice. C and D: Western blot analyses (C) and quantification (D) of renin protein levels in the kidney of all mice as indicated. #P < 0.05, ##P < 0.01 vs. C. *P < 0.05 vs. L. E and F: RT-PCR determination of mRNA levels (E) and quantification (F) of angiotensinogen (AGT), angiotensin-converting enzyme (ACE), the (pro)renin receptor (ReninR), and AT₁ receptor (AT1R) in the kidney. B2M served as an internal control. *P < 0.05, **P < 0.01 vs. L. #P < 0.05, ##P < 0.01 vs. C; n = 6–7. G: intrarenal ANG II accumulation determined by immunostaining. Nondiabetic mice (C) and diabetic mice treated with V, L, DL, L+DL, or L+DH were killed at week 20, and kidney sections from these mice were stained with an ANG I/II-specific antibody. Note strong staining in both the glomerular (indicated by an arrow) and tubular areas in L-treated kidney.