Abstract P100: (Pro)renin Receptor (PRR) Mediates Renal Inflammation in Renovascular Hypertension
We hypothesized that PRR plays a role in renal inflammation in 2-kidney, 1-clip (2K1C) hypertension rat model. Male Sprague-Dawley rats were fed normal sodium diet. BP was obtained before and 28 days after left renal artery clipping. Renal expressions of PRR, TNF-α and COX-2 were assessed in sham and 2K1C rats with or without left renal interstitial administration of scramble shRNA or PRR shRNA. At baseline there were no significant differences in BP between different animal groups. Compared to sham, mean arterial blood pressure significantly increased in 2K1C (2K1C 131.8 ± 3.09 mmHg, vs. sham 108 ± 1.9 mmHg, P<0.0.05) at day 28 and was not influenced by scramble shRNA or PRR shRNA treatment. Compared to sham and contra lateral (non-clipped) kidney, there were increases in mRNA and protein expressions of PRR (90% and 45%, P<0.01), TNF-α (72% and 50%, P<0.05), COX-2 (72% and 39%, P<0.05) in the clipped kidney. These expressions were not influenced by scramble shRNA treatment. Compared to 2K1C (no treatment) and scramble shRNA, PRR shRNA treatment in the clipped kidney caused significant reductions in mRNA and protein expressions of PRR (60% and 54%, P<0.01, shown in figure below), TNF-α (54% and 51%, P<0.05), COX-2 (51% and 53%, P<0.05). We conclude that PRR mediates renal inflammation in renovascular hypertension independent of blood pressure reduction.
Author Disclosures: S. Quadri: None. C. Li: None. S. Culver: None. H.M. Siragy: None.
- © 2015 by American Heart Association, Inc.