盐酸贝那普利对自发性高血压大鼠肾脏纤维化的影响  

Effect of benazepril on renal fibrosis in spontaneously hypertensive rats

作　　者：王先梅[1] 杨丽霞[1] 宋武战[2] 齐峰[1] 郭传明[1] 石燕昆[1] 赵颖[1] 魏玲[1] 王燕[1] 

机构地区：[1]成都军区昆明总医院心血管内科,云南昆明650032 [2]成都军区昆明总医院核医学科,云南昆明650032

出　　处：《第四军医大学学报》2006年第20期1859-1862,共4页Journal of the Fourth Military Medical University

摘　　要：目的:观察血管紧张素转换酶抑制剂(ACEI)对自发性高血压大鼠(spontaneously hypertensive rats,SHR)肾内肾素—血管紧张素系统(RAS)的影响,探讨盐酸贝那普利抗肾脏纤维化的机制.方法:应用病理检查、计算机分析、放射免疫、分光光度法和逆转录—聚合酶链式反应等方法,检测贝那普利组(SHR-B)、SHR组(SHR)及对照Wistar-Kyoto组(WKY)大鼠肾脏间质胶原面积、肾脏血管紧张素转换酶(ACE)活性、肾脏局部血管紧张素II(Ang II)水平及肾脏组织I,III型胶原mRNA表达.结果:SHR-B组肾脏胶原面积比SHR组明显减少(P<0.01).SHR-B组肾皮质提取液ACE活性为(28±6)nmol/(min·g),SHR组为(53±8)nmol/(min·g),WKY组为(25±7)nmol/(min·g).SHR-B组肾皮质提取液ACE活性比SHR组明显降低(P<0.01),但与WKY组相比,无显著差异.SHR-B组肾皮质组织匀浆液Ang II水平为(49±16)ng/g,SHR组为(83±8)ng/g,WKY组为(43±14)ng/g.SHR-B组肾皮质组织匀浆液Ang II水平比SHR组明显降低(P<0.01),但与WKY相比无显著差异(P>0.05).SHR-B组肾脏组织I型胶原及III型胶原mRNA表达相对含量也均明显低于SHR组(P均<0.01).结论:贝那普利可通过减少肾脏胶原的合成和抑制肾内的RAS而减轻肾脏的纤维化.AIM： To observe the effect of angiotensin-converting enzyme inhibitor （benazepril） on intrarenal renin-angiotensin system （RAS） in spontaneously hypertensive rats （SHR） and to explore the mechanism by which benazepril protects kidney from renal interstitial fibrosis. METHODS： The animals were randomly divided into 3 groups： spontaneously hypertensive rats treated with benazepril （SHR-B） group and SHR group and WistarKyoto （WKY） group. Using the methods of pathological examination and computer processing, the renal collagen area in kidney was observed. The area of collagen was examined by the image analysis system. The renal local angiotensin-eonverting enzyme （ACE） activity was detected by ultra-violet spectrophotography. Renal angiotensin Ⅱ （Ang Ⅱ） concentration was measured by radioimmunoassay. The mRNA expressions of type Ⅰ- and type Ⅲ- collagens in renal tissue were analyzed using the reverse transcriptase-polymerase chain reaction （ RT - PCR ）. RESULTS ： The area of collagen was significantly decreased in SHR-B group compared to SHR group （P 〈0. 01 ）. The renal local ACE activities were （27.6 ±6.5） nmol/（ min·mg） in SHR-B group and （53.4±8.2） nmol/（min·mg） in SHR group and （25.3 ±6.9） nmol/（min·mg） in WKY group; there was a significant decrease in SHR-B group as compared with SHR group （ P 〈 0.01 ）, and there was no significant difference between SHR-B and WKY groups （ P 〉 0. 05 ）. The contents of Ang Ⅱ in renal local tissue were also markedly lower in SHR-B group than in SHR group[ （49.3 ±16.1） ng/gvs （83.4±8.2） ng/g, P〈0.01） ]. There was no significant difference between SHR-B and WKY （P 〉 0.05）. The relative levels of mRNA expressions of type Ⅰ- and type Ⅲ- collagens in renal tissue were markedly lower in SHR-B group than in SHR group （P 〈0.01, respectively）. CONCLUSION： Benazepril could attenuate rat renal fibrogenesis by inhibiting the activity of the renal RAS and decreasi

关 键 词：血管紧张素转换酶抑制药 肾素-血管紧张素系统 肾脏纤维化 胶原 

分 类 号：R692[医药卫生—泌尿科学]