In this study, AT1R expression was markedly up-regulated in the heart failure group, while AT2R expression was significantly down-regulated, suggesting changes of ATR expression levels in the kidney during CHF, which could contribute to renal interstitial edema, inflammatory cell infiltration, glomerular fibrosis, and tubular necrosis, ultimately affecting renal perfusion and reserve function [18, 19]. Here, ATR is linked to congestive heart failure.