中文摘要：

目的：探讨肾脏局部肾素-血管紧张素系统（renin-agiotensin system,RAS）在高盐诱发大鼠高血压及其肾损害发病机制中的作用。方法：8周龄雄性Wistar大鼠随机分为3组：对照组（NS,n=9）,普通饲料喂养;高盐组（HS,n=9）,含8%（质量分数）Na Cl的高盐饲料喂养;高盐饮食＋氯沙坦组（HS＋L,n=9）,高盐饲料喂养同时每日给予氯沙坦20 mg/kg灌胃。实验共6周,期间每2周监测血压和24 h尿蛋白,6周后处死大鼠,放射免疫法测定血浆、肾脏匀浆以及尿液的肾素活性、血管紧张素Ⅱ水平,Real-time PCR、免疫组织化学染色分别检测肾脏血管紧张素原（angiotensinogen,AGT）mRNA、蛋白表达水平,ELISA测定血、肾皮质匀浆液以及尿AGT水平。结果：与NS组相比,HS组大鼠第2周始血压显著升高[（156±2）mm Hg vs.（133±3）mm Hg（1 mm Hg=0.133 k Pa）,P〈0.05）],第6周时尿蛋白显著增加[（14.07±2.84）mg/24 h vs.（7.62±3.02）mg/24 h,P〈0.05];HS＋L组与HS组大鼠血压差异无统计学意义（P〉0.05）,但第6周时HS＋L组尿蛋白比HS组显著降低[（9.69±2.73）mg/24 h vs.（14.07±2.84）mg/24 h,P〈0.01]。与NS组相比,HS组血浆肾素活性、AGT和血管紧张素Ⅱ（angiotensinⅡ,ANGⅡ）水平无显著变化（P〉0.05）,肾皮质肾素活性、AGT和ANGⅡ水平均显著升高（P〈0.05）,尿AGT和ANGⅡ排泄率均显著升高（P〈0.05）;与HS组相比,HS＋L组大鼠血浆肾素活性、AGT和ANGⅡ水平均显著升高（P〈0.05）,肾皮质肾素活性、ANGⅡ和AGT水平均显著降低（P〈0.05）,尿AGT和ANGⅡ排泄率均显著降低（P〈0.01）,尿AGT排泄率与肾皮质AGT水平呈显著正相关（P〈0.05）。结论：高盐可能通过上调肾脏局部RAS的表达参与大鼠的肾损害,尿AGT排泄率可能反映肾脏局部RAS激活的程度。

英文摘要：

Objective： To test the hypothesis that in a high-salt induced hypertension in normal rats,whether the changes of intrarenal renin-agiotensin system（ RAS） play a critical role in renal damage and could be reflected by urinary angiotensinogen（ AGT）. Methods： In the study,27 normotensive male Wistar-Kyoto rats were divided into control group [0. 3%（ mass faction） Na Cl in chow,n = 9,NS],high-salt diet group [8%（ mass faction） Na Cl in chow,n = 9,HS] and high-salt diet with Losartan group [8%（ mass faction） Na Cl in chow and 20 mg /（ kg·d） Losartan in gavages,n = 9,HS ＋ L） ],and were fed for six weeks. The blood pressure was monitored and urine samples were collected every 2weeks. AGTs in plasma,kidney and urine were measured by ELISA kits. The renal cortex expression of mRNA and protein of AGT were measured by Real-time PCR and immunohistochemistry（ IHC）. The renin activity and ANG Ⅱ were measured by radioimmunoassay（ RIA） kits. Results： Compared with NS,the systolic blood pressure（ SBP） [（ 156 ± 2） mm Hg vs.（ 133 ± 3） mm Hg,P 〉0. 05] increased significantly at the end of the 2nd week,and the urinary protein [（ 14. 07 ± 2. 84） mg /24 h vs.（ 7. 62 ±3. 02） mg /24 h,P 〉0. 05] increased significantly at the end of the 6th week in HS. Compared with HS,there was no significant difference in SBP（ P 〉0. 05） but the proteinuria [（ 9. 69 ± 2. 73） mg /24 h vs.（ 14. 07 ± 2. 84） mg /24 h,P〈 0. 01] decreased significantly in HS ＋ L. Compared with NS,there was no significant difference in the plasma renin activity,angiotensinogen and ANGⅡ level in HS（ P 〉0. 05）,but the renal cortex renin content [（ 8. 72 ± 1. 98） ng /（ m L·h） vs.（ 4. 37 ± 1. 26） ng /（ m L·h）,P 〉0. 05],AGT formation [（ 4. 02 ± 0. 60） ng / mg vs.（ 2. 59 ± 0. 42） ng / mg,P〈 0. 01],ANGⅡ level [（ 313. 8 ± 48. 76） pmol /L vs.（ 188. 9 ± 46. 95） pmol /L,P 〉0. 05] were increased significantly in HS,and the urinary AGT and ANG?