Abstract: Abstract: Objective To investigate the effect of enalapril on angiotensin (Ang) Ⅱ and TGF-β/Smads in renal tissue
of spontaneously hypertensive rats (SHR). Methods A total of 20 male SHRs were randomly divided into model group and
enalapril group. Ten male Wistar Kyoto rats (WKY) were taken as control group. The dosage of enalapril was 1.05 mg/(kg·d),
once a day, for 10 weeks. The model group and the control group were given the same amount of normal saline. Blood
pressure was monitored every two weeks regularly. After 10 weeks animals were killed and tissue samples were collected.
Urease method was used to detect the blood urea nitrogen (BUN) content. Enzyme-linked immunosorbent assay (ELISA) was
used to detect the contents of Ang Ⅱ, serum cystatin C (CysC) and urinary microalbumin (mALB). Masson staining was used
to observe the renal pathological changes. Real-time PCR was used to detect the relative mRNA expressions of Ang Ⅱ ,
transforming growth factor β1(TGF-β1), Smad2, Smad3, CollagenⅠ and Collagen Ⅳ. Results Compared with the control
group, the systolic and diastolic blood pressures increased significantly in the model group and enalapril group (P＜0.05).
There were no significant differences in the systolic and diastolic blood pressures between the model group and enalapril
group (P＞0.05). After drug intervention, compared with the model group, the systolic and diastolic blood pressures
decreased significantly in enalapril group (P＜0.05). Compared with the control group, the levels of Ang Ⅱ, BUN, CysC and
urinary mALB were significantly increased in the model group (P＜0.05). A large number of blue collagen fibers were
deposited in renal tissue, and the relative mRNA expressions of Ang Ⅱ, TGF-β1, Smad2, Smad3, Collagen Ⅰ and Collagen
Ⅳ were significantly increased (P＜0.05). Compared with the model group, the level of collagen deposition was significantly
reduced in renal tissue, and the above indexes in serum and kidney decreased significantly in enalapril group (P＜0.05).
Conclusion Enalapril has a stable hypertensive effect on SHR, and it can alleviate renal fibrosis and improve renal injury
caused by hypertension by lowering Ang Ⅱ level and inhibiting the expression of TGF-β/Smads signaling pathway.

Key words: Enalapril, rats, inbred SHR, angiotensinⅡ, transforming growth factor beta, renal fibrosis