复合离子盐对高血压大鼠肾脏皮质AngⅡ、NO的产生及磷酸化ERK1/2表达的影响  

Effects of Compound-ion Salt on Generation of AngⅡ,NO and Expression of Phosphorylated ERK1/2 in Renal Cortex of Spontaneously Hypertensive Rats

作　　者：庞伟[1] 石蕊[1] 李玉明[1] 

机构地区：[1]武警医学院附属医院心血管病研究所,天津300162

出　　处：《中国微循环》2008年第2期93-96,共4页Journal of Chinese Microcirculation

基　　金：天津市科技发展计划项目(NO023181411)

摘　　要：目的观察复合离子盐对自发性高血压大鼠(SHR)肾脏皮质AngⅡ、NO的产生,及对磷酸化ERK1/2(p-ERK1/2)表达的影响,探讨复合离子盐对SHR肾脏保护作用的可能机制。方法42只8周龄雄性SHR随机分为4组:8%食盐摄入组(HS组);1%复合离子盐摄入组(CIS组);1%复合离子盐+2.25%L-精氨酸摄入组(CIS+L-Arg组);1%食盐摄入组(NS组),持续干预12周。干预期间定期观察大鼠血压、尿蛋白的变化;干预结束后处死动物,放射免疫法检测肾皮质中AngⅡ、NO含量;并通过Western-blot法分析SHR肾脏皮质磷酸化ERK1/2蛋白表达的情况。结果12周干预结束后,CIS组与CIS+L-Arg组血压升高趋势明显低于NS组(P<0.01)。CIS组与CIS+L-Arg组尿蛋白排泄量与实验前相比无差异,但显著低于NS组(P<0.01)。与NS组相比,CIS组与CIS+L-Arg组可明显促进SHR肾脏组织NO的生成(P<0.01),抑制组织AngⅡ的产生(P<0.01),同时p-ERK1的表达在CIS组与CIS+L-Arg组明显降低(P<0.05)。结论复合离子盐与普通食盐比较,长期同等量摄入时可通过改变肾皮质中AngⅡ、NO含量,改善其功能平衡,还可使ERK1/2信号传导通路发生改变,这可能改善盐诱导的靶器官损害作用。Objective To investigate the effects of compound-ion salt on the generation of Ang Ⅱ, NO and the expression of phosphorylated ERK1/2（p-ERK1/2） in renal cortex of spontaneously hypertensive rats （SHR）. Methods 42 male SHR of eight weeks were randomized to receive 8% high salt（ HS group） ; 1% compound-ion salt（ CIS group） ; 1% compound-ion salt plus 2.25% L-Arg（ CIS ＋ L-Arg group） ; and 1% normal salt（NS group） for 12 weeks. Throughout the experiments, systolic blood pressure and urinary protein ex cretion were measured every three weeks. After intervention, all rats were sacrificed, and then blood was col- lected. The contents of AngⅡ and NO in renal cortex were measured by radioimmunoassay（ RIA）. The protein expression of p-ERK1/2 in cortex of kidney was analyzed by Western blot. Results Compared with normalsalt diet, 1% compound-ion salt or 1% compound-ion salt ＋2.25% L-Arg intake could promote the produc- tion of NO in cortex of kidney（P 〈0.01）, and inhibit the production of AngⅡ in cortex（P 〈 0. 01）. At the same time, compound-ion salt and compound-ion salt ＋ L-Arg intake decreased the protein expression of p- ERK1 in renal tissue （ P 〈0. 05）. Conclusion Compound-ion salt intake could maintain the balance between Ang Ⅱ and NO and influence the protein expression of p-ERK1/2, so it could ameliorate target-organ damage induced by sodium.

关 键 词：盐 高血压 AngⅡ NO ERK1/2 靶器官损害 

分 类 号：R544.1[医药卫生—心血管疾病]