Angiotensin Ⅱ regulates Aquaporin 2 expression after bilateral ureteral obstruction in rats
WANG Yan, WEN Jian-guo, ZHANG Rui, LI Zhen-zhen, XING Lu, WANG Qing-wei, ZHANG Guo-xian, Lou An-feng
Published 2011-09-15
Cite as Chin J Pediatr Surg, 2011,32(09): 696-700. DOI: 10.3760/cma.j.issn.0253-3006.2011.09.014
Abstract
Objective To investigate the regulation of angiotensin Ⅱ on the expression of Aquaporin 2 (AQP2) and renal function after bilateral ureteral obstruction (BUO). Methods Tweentyfour Munich-Wistar rats were randomly divided into three groups (BUO, n = 8; CAN n = 8; Sham n =8). The BUO (and BUO + CAN) model was built by bilateral ureteral ligation, then the osmotic minipumps contained isotonic saline (n = 8) or candesartan (n = 8) were implanted subcutaneously.Age-and time-matched sham-operated controls (n = 8) were prepared and observed in parallel. The rats were monitored for another 48 h after the 24 h BUO was released. The blood samples were collected and kidneys were harvested to examine the effects of angiotensin Ⅱ receptor antagonist candesartan on the dysregulation of AQP2 by semi quantitative immunoblottling. Results Release of BUO resulted in a marked polyuria(BUO vs. Sham: 92 ± 7 vs. 25 ± 3μl min 1 kg-1 ,n = 8;P＜0. 05) and a reduced urine osmolality(BUO vs. Sham: 636 ± 55 vs. 1 853 ± 163 mosmol/kgH2O,n = 8; P＜0. 05) ,which persisted throughout the experimental period. Administration of candesartan partly prevented this increase in postobstructive urine production (55 ± 5 vs. 92 ± 7 μl min-1 kg 1, n = 8 ; P＜0. 05) and decrease in urine osmolality (783 ±47 vs. 636 ± 55 mosmol kgH2O-1 ,n = 8; P＜0. 05). BUO induced a significantly increase in plasma osmolality (336 ± 10 vs. 303 ± 7 mosmol/kgH2O,n = 8; P＜0. 05) and plasma aldosterone concentration (4. 1 ±0. 2 vs. 1.4±0. 1 nmol L-1 ,n= 8; P＜0. 05) in BUO vs. In shamoperated control rats. Candesartan partly attenuated the increase of plasma aldosterone (2. 8 ± 0. 5 vs.4. 1 ± 0. 2 nmol L-1, n = 8; P＜0. 05). BUO resulted in a significantly decreased expression of AQP2compared with control,and candesartan prevented the reduction of AQP2 (P＜0. 05). Conclusions Angiotensin Ⅱ receptor antagonist prevents dysregulation of AQP2 in response to BUO. Angiotensin Ⅱ is involved in the pathophusilogical changes in renal function after release of BUO.
Key words:
Bilateral ureteral obstruction; Aquaporin 2; Angiotensin Ⅱ type I receptor blockers
Contributor Information
WANG Yan
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
WEN Jian-guo
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
ZHANG Rui
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
LI Zhen-zhen
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
XING Lu
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
WANG Qing-wei
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
ZHANG Guo-xian
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
Lou An-feng
Urodynamic Center, Department of Urology, The First Affiliated Hospital, Zhengzhou University, Institute of Clinical Medical Research of Universities Henan Province, Zhengzhou 450052, China
