摘要
目的观察坎地沙坦干预对双侧输尿管梗阻（BUO）大鼠肾功能和Na—K-2Cl共转运蛋白2（NKCC2）的影响。方法30只大鼠随机分为假手术（Sham）、BUO和坎地沙坦干预组（BUO＋CAN）。BUO组和（BUO＋CAN）组均行BUO手术，（BUO＋CAN）组坎地沙坦干预，24h后解除梗阻再观察48h收集血液、肾脏标本。免疫印迹实验检测肾脏NKCC2表达水平。结果梗阻解除后BUO与Sham组比较尿量、尿Na增高[（99±6）ul／（min·kg）比（28±4）ul／（min·kg）]和[（7．0±0．7）umol／（min·kg）比（4．0±0．4）umol／（min·kg）]，尿渗透压降低，血浆渗透压、醛固酮升高。BUO＋CAN与BUO组比较尿量、尿Na降低[（60±7）ul／（min·kg）比（99±6）uL／（min·kg）]和[（4．9±0．4）umol／（min·kg）比（7．0±0．7）umol／（min·kg）]，尿渗透压增高，血浆渗透压、血浆醛固酮降低。NKCC2表达BUO组下降到Sham组的24％，（BUO＋CAN）组高于BUO组[（58±6）％比（24±7）％]。各组比较差异均有统计学意义（P〈0．05）。结论坎地沙坦可阻止BUO后NKCC2下调，纠正代谢紊乱，保护肾功能。
Objective To investigate the effects of candesartan （CAN） on dysregulation of Na-K-2Cl cotransporter 2 （NKCC2） and renal function in response to bilateral ureteral obstruction （BUO）. Methods Thirty Munich-Wistar rats were randomly divided into three groups （BUO, BUO ＋ CAN and sham）. The BUO model was built by bilateral ureteral ligation, then the BUO ＋ CAN rats were treated with CAN. The kidneys were harvested for semi-quantitative immunoblotting. Results BUO induced an increase in plasma osmolality [ BUO vs. sham ： （340 ± 8 ） vs. （ 305 ± 9 ） mosmol/kg H2 O, P 〈 0. 05 ] and plasma aldosterone concentration [ BUO vs. sham： （4. 5 ±0. 2） vs. （ 1.4 ±0. 1 ） nmol/L,P 〈 0. 05 ] in BUO vs. sham group. Administration of CAN partly prevented this increase in postobstructive urine production [ BUO ＋ CAN vs. BUO ： （ 60 ± 7 ） vs. （99 ± 6 ） ul/（ min. kg） ,P 〈 0. 05 ] , increase of urine Na [ BUO ＋ CAN vs. BUO ： （4.9 ± 0. 4） vs. （7.0 ± 0. 7 ） umol/（ min. kg）, P 〈 0. 05 ] and decrease in urine osmolality [ BUO ＋ CAN vs. BUO ： （ 806 ± 61 ） vs. （ 647 ± 57 ） mosmol/kg H2 O, P 〈 0. 05 ]. CAN attenuated partly the increase of plasma osmolality and aldosterone [ BUO ＋ CAN vs. BUO ： （ 325 ± 7） vs. （340 ± 8） mosmol/kg H2O and （2. 9 ± 0.4） vs. （4. 5 ± 0. 2） nmol/L, P 〈 0. 05 ]. BUO resulted in a significandy decreased expression of NKCC2 compared with sham group, and CAN prevented the reduction of NKCC2 （ P 〈 0.05 ）. Conclusion Angiotensin II receptor antagonist prevents dysregulation of NKCC2 in response to BUO, which is likely to contribute to the associated urinary concentrating defect.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2012年第6期1034-1036,共3页
Chinese Journal of Experimental Surgery
基金
基金项目：河南省医学科技攻关计划资助项目（200801002）
