Objective To investigate the changes in renal functions and the renin-angiotensin system (RAS) at different stages in endotoxemia rats, to provide data to support its pathological mechanism. Methods Ninety rats were randomly divided into nine groups: the control group (n= 10) and the model group at eight timepoints (2, 4, 8, 12, 24, 48, 72 and 168 h, n= 10). Rats in the model group were prepared for the sepsis model by a tail vein injection of lipopolysaccharides, while those in the control group were injected with an equal volume of pyrogen-free water. Samples were collected from the animals in the control group at 8 h after injection and from animals in the model group at each timepoint. The circulating endotoxin, nitric oxide (NO), endothelin ( ET), nitric oxide synthase (NOS), angiotensin converting enzyme (ACE), angiotensin (Ang), renin-angiotensin (PRA), serum creatinine and blood urea nitrogen levels were detected by enzyme-linked immunosorbent assay, the protein expression of AngII type 1 receptor (AT1R) and Ang II type 2 receptor ( AT2R) in the kidney was measured using Western blot assay. Results After lipopolysaccharide injection, the circulating endotoxin, endothelin, NO, NOS, ACE, AngⅡ, serum creatinine, blood urea nitrogen, AT1R and AT2R levels were all increased in the model group. The kidney coefficient, serum endotoxin, serum creatinine, blood urea nitrogen and kidney AT1R and AT2R were higher in the model group than in the control group at 2 ~ 168 h after injection. In addition, the serum levels of endothelin, NOS and AngⅡ were higher in the model group than in the control group at 2~ 48 h after injection and the NO level in the model group was higher than that in the control group at 4 ~ 48 h after injection. Moreover, the ACE level in the model group was higher than that in the control group at 2 ~ 24 h after injection. All differences were significant ( P< 0. 05). Conclusions RAS may be involved in kidney injury caused by endotoxemia.