急性肾功能衰竭患者血浆PRA、AT-Ⅱ和Ald水平变化的临床分析

目的 :为了探讨血浆PRA、AT -Ⅱ和Ald在急性肾功能衰竭发病机理中的作用。方法 :我们应用放射免疫分析测定了 4 0名正常人和 72例急性肾功能衰竭病人血浆中的PRA、AT -Ⅱ和Ald的水平。结果 :72例急性肾功能衰竭病人血浆PRA、AT -Ⅱ和Ald明显高于 4 0名正常人 (p <0 0 5、p<0 0 1和p<0 0 0 1) ,普食卧位血浆PRA、AT -Ⅱ和Ald与 2 4h尿钠排出量为 89 1～ 36 5 2毫克当量的范围内无直线和指数的关系。结论 :急性肾功能衰竭具有激活RAAS的作用     

内皮素-1与血管紧张素Ⅱ在慢性环孢素A肾病大鼠中的作用

慢性环孢素A(CsA)肾病的具体发生机制尚不明确,CBA可增加血肾素、血管紧张素Ⅱ(AngⅡ)的活性,肾素-血管紧张素系统(RAS)的激活可能是其发生机制之一[1].     

新生儿缺氧缺血性脑病时血浆肾素,血管紧张素Ⅱ,醛固酮的变化

采用放射免疫法测定４０例新生儿缺氧缺血性脑病患儿的血浆肾素、血管紧张素Ⅱ、醛固酮水平。结果显示：ＰＲＡ无明显变化,急性期轻度ＨＩＥ的ＰＡⅡ（２０１．３４±５．３８Ｐａ／ｍｌ）、ＰＡＬＤ（０．３６２±０．１０７）与中重度ＨＩＥ的ＰＡⅡ（３６２．３４±７５．１５Ｐａ／ｍｌ）、ＰＡＬＤ（０．５４３±０．１５２ｎｇ／ｍｌ比较,无有显差异（ｔ＝２．８１３,Ｐ〈０．０５;ｔ＝３．１０１,Ｐ〈０．０５）,并且     

肝硬化腹水时血钠与血浆心钠素,肾素,醛固酮变化的探讨

近年来,国内外文献报道肝硬化腹水与心钠素(ANP)、肾素(PRA)和醛固酮(ALD)的关系密切。因此,我们对本院近2年住院的89例肝硬化腹水患者进行检测,并观察ANP、PRA和ALD与血钠、肾功能的关系,现报道如下。 资料和方法 肝硬化组89例(男68,女21例),均为住院患者,年龄22～83岁,平均51.75岁。均据临床表现和B超、CT等各种辅助检查确诊为肝硬化并腹水。其中肾功能异常和发生肝肾综合征者20例。健康对照组     

Role of angiotensin Ⅱ and JAK2 signal pathway in transdifferentation of renal tubular cells in mice after acute ischemic followed by reperfusion

Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway.     

ACE/ACE2在AGT-REN双转基因高血压小鼠肾组织的表达变化及意义

目的: 观察血管紧张素原(AGT)-肾素(REN)双转基因高血压小鼠肾脏组织病理改变及血管紧张素转化酶(ACE)/血管紧张素转化酶2(ACE2)的表达变化,探讨ACE和ACE2在高血压肾损伤中的作用。方法: 实验分为4组,随机选择10月龄野生型、AGT转基因、REN转基因以及AGT-REN双转基因雄性C57小鼠各6只。每组动物颈动脉插管检测平均动脉压(MAP),1 h后处死小鼠;左侧肾脏置于10%中性甲醛固定,常规HE染色方法观察肾脏组织病理改变,免疫组化法观察肾脏ACE及ACE2的表达变化;右侧肾脏取出后放入蛋白裂解液中,提取蛋白,进行Western blotting实验,观察肾组织中ACE和ACE2蛋白表达。结果: 与野生型小鼠相比,AGT转基因小鼠MAP无明显变化(P>0.05),REN转基因小鼠MAP降低约15 mmHg(P<0.05);AGT-REN双转基因小鼠MAP明显升高约30 mmHg(P<0.05)。与野生型小鼠相比,AGT转基因和REN转基因小鼠肾组织未见明显病理改变,AGT-REN双转基因小鼠肾组织可见肾小动脉内膜及管壁显著增厚、管腔狭窄、纤维素样坏死、玻璃样变等典型恶性高血压肾损伤病理改变。免疫组化结果显示,与野生型小鼠相比,AGT转基因和REN转基因小鼠肾组织ACE和ACE2表达无明显差异(P>0.05),AGT-REN双转基因鼠肾组织ACE表达明显增高(P<0.05),而ACE2表达明显降低(P<0.05)。Western blotting结果显示:与野生型小鼠相比,AGT转基因鼠肾组织ACE和ACE2表达无明显变化;REN转基因鼠肾组织ACE表达无明显变化,ACE2表达稍降低(P<0.05);双转基因鼠肾组织ACE蛋白表达明显增强, ACE2蛋白表达水平显著降低,ACE/ACE2表达显著失衡。结论: AGT-REN双转基因可致小鼠恶性高血压,导致肾脏严重损伤;ACE/ACE2的表达失衡与血压改变密切相关,降低ACE或提高ACE2的表达可能对防治高血压具有重要意义。     

肢体缺血再灌注后肺损伤小鼠肺组织AT1R和Mas受体蛋白表达变化

目的:通过观察小鼠肢体缺血再灌注(LIR)后不同时点肺组织血管紧张素Ⅱ1型受体(AT1R)和Mas受体蛋白表达与肺损伤的变化,探讨局部组织AT1R和Mas受体蛋白表达失衡在LIR急性肺损伤(ALI)中的作用。方法:42只8周龄雄性ICR小鼠随机分为7组,每组6只,其中1组作为对照组,其余6组为再灌注0.5 h、1h、2 h、4 h、6 h和12 h模型组。模型组小鼠用橡皮圈结扎双后肢根部,缺血2 h后剪断橡皮圈,分别于再灌注后不同时点眼球取血处死小鼠。取肺组织计算脏器系数和湿/干重比;肺泡灌洗液细胞计数和蛋白浓度检测;肺组织病理切片常规HE染色观察肺组织形态变化并进行病理损伤评分;Western blot检测肺组织AT1R和Mas受体蛋白的表达。结果:模型组小鼠肺脏器系数、湿/干重比、肺泡灌洗液细胞计数和蛋白浓度在LIR后显著升高。病理学结果显示,LIR后不同时点小鼠肺组织出现肺泡壁毛细血管扩张和充血、间质和肺泡水肿、血管壁和支气管壁炎症细胞浸润、肺泡间隔增厚、炎症细胞浸润及肺气肿等不同程度的损伤变化,且随着再灌注时间的延长,肺损伤评分逐渐升高。Western blot结果显示,AT1R蛋白在再灌注0.5 h时开始升高,1 h达到最高,之后随再灌注时间的延长,AT1R表达逐渐降低;Mas受体蛋白随再灌注时间延长逐渐升高。结论:LIR引起急性肺损伤,并随再灌注时间的延长损伤逐渐加重;AT1R和Mas受体蛋白表达的变化可能与小鼠LIR后急性肺损伤有关。     

血管紧张素Ⅱ受体拮抗剂的临床研究进展

血管紧张素受体拮抗剂能特异性地与血管紧张素Ⅱ受体结合 ,从而可以阻断所有已知与高血压和心血管并发症有关的血管紧张素Ⅱ作用 ,其治疗高血压的疗效与目前一线降压药物相同 ,但不良反应低。     

Role of angiotensin Ⅱ and JAK2 signal pathway in transdifferentation of renal tubular cells in mice after acute ischemic followed by reperfusion

Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway.