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目的:探讨肾特异性钙粘素(ksp)表达异常导致盐敏感性高血压的机制。方法:选择30只Dahl/ss大鼠,将其分为模型+药物组、模型组、空白组,每组各10只,模型+药物组及模型组给予8%食盐饲料喂养制备盐敏感性高血压大鼠模型,造模成功后分别给予补肾方水煎剂、蒸馏水灌胃5周。检测各组体质量、肾脏脏器指数、血清尿素氮(BUN)、血肌酐(Scr)、总蛋白(Tp)、血白蛋白(Alb)、尿蛋白、尿NAG及ksp含量。结果:3组体质量、肾脏脏器指数、Scr比较,差异均无统计学意义(P>0.05);与模型+药物组和空白组相比,模型组血BUN、尿蛋白、尿NAG、ksp平均光密度升高(P<0.05);与空白组相比,模型+药物组和模型组血Tp、Alb含量降低(P<0.05)。结论:高盐饮食会造成肾特异性钙粘素的表达异常,从而形成肾小管间质损伤,导致盐敏感性高血压。
Objective: To investigate the mechanism of abnormal renal expression of cadherin (ksp) leading to salt-sensitive hypertension. Methods: Thirty Dahl / ss rats were selected and divided into model group, drug group, model group and blank group, with 10 rats in each group. The rats in model group and drug group were fed with 8% salt diet to prepare salt-sensitive Blood pressure rat model, respectively, after modeling successful kidney Bushen Decoction, distilled water for 5 weeks. Body mass, index of kidney organ, serum urea nitrogen (BUN), serum creatinine (Scr), total protein (Tp), albuminuria (ALB), urinary protein, urinary NAG and ksp were detected. Results: There was no significant difference in body mass, kidney organ index and Scr between the three groups (P> 0.05). Compared with the model group and the blank group, blood BUN, urinary protein, urinary NAG, ksp (P <0.05). Compared with the blank group, the content of Tp and Alb in model + drug group and model group decreased (P <0.05). CONCLUSIONS: High-salt diet causes abnormal expression of renal-specific cadherins, resulting in tubulointerstitial injury leading to salt-sensitive hypertension.