Expression of angiotensin Ⅱ and its type 1 receptor in circulation, placenta and kidney of the preeclampsia rat model
- VernacularTitle:先兆子痫大鼠循环、胎盘及肾脏局部血管紧张素Ⅱ及其1型受体的表达
- Author:
Lin TAO
;
Jianying NIU
;
Li YOU
;
Jing CHEN
;
Yong GU
- Publication Type:Journal Article
- Keywords:
Preeclampsia;
Proteinuria;
Kidney damage;
Angiotensin Ⅱ;
AT1
- From:
Chinese Journal of Nephrology
2008;24(9):663-668
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of angiotensinⅡ (Ang Ⅱ ) and its type 1 receptor (AT1) in circulation, placenta and kidney of the rots preeclampsia. Methods Preedampsia rat model was developed by inhibitor of nitric oxide synthase (L-NAME). The systolic blood pressure (SBP), 24 h urine protein, hepatic and renal function were compared among the precelampsia group, the normal pregnant group and nonpregnant control group. The kidney tissue was observed by light microscopy. ELISA and radioimmunoassay were used to detect Ang Ⅱ in rat plasma and kidney homogenate respectively. Placental AT1 was measured by Westem blot. The level of kidney AT1 was evaluated by immunohistochemistry and Western blot. Results In preeclampsia rats, SBP and 24 h urine protein were significantly higher compared with control groups. Compared to normal pregnant group, plasma Ang Ⅱ of preeclampsia rats was much higher [(0.706±0.086) ng/L vs (0.540±0.085) ng/L, P＜0.05]; placental AT1 was increased by 46%(P＜ 0.05); kidney Ang Ⅱ was decreased signigicantly [(65.543±40.634) ng/g vs (165.543±33.078) ng/g, P＜0.05]. The expression of ATI in kidney of preeclampsia rats was reduced evidently,which was only 33% of normal pregnancy group and 59% of nonpregnant control greup,respeetively (P＜0.05). Conclusions In preeclampsia rat model, the circulating Ang Ⅱ is increased, the placental RAS isactivated, while the kidney BAS is suppressed. The underlying mechanism of proteinuria and kidney damage associated with this phenomenon in preeclampsia needs further research.
