中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2013年
4期
276-281
,共6页
心力衰竭,充血性%水通道蛋白质2%培哚普利
心力衰竭,充血性%水通道蛋白質2%培哚普利
심력쇠갈,충혈성%수통도단백질2%배타보리
Heart failure,congestive%Aquaporin-2%Perindopril
目的 探讨慢性心力衰竭(心衰)大鼠肾脏水通道蛋白2(aquaporin-2,AQP2)表达和尿液AQP2浓度的变化,及培哚普利对其的影响.方法 雄性SD大鼠60只,按照简单随机化分组法分为对照组、生理盐水组和培哚普利组,每组20只.建立大鼠心衰模型,生理盐水组、培哚普利组大鼠左心室梗死面积(left ventricular myocardial infarction size,LVMI)≥20％者选入各自心衰亚组,LVMI＜20％者选入各自心功能代偿亚组.干预后检测大鼠血压、血钠浓度、尿量以及尿渗透压,免疫组织化学、逆转录-聚合酶链反应(RT-PCR)、蛋白质印迹法(Western blot)法检测大鼠肾脏AQP2 mRNA和蛋白的表达情况,放射免疫法检测血浆血管加压素(arginine vasopressin,AVP)的浓度,间接ELISA法检测尿液AQP2的浓度.结果 生理盐水组心衰亚组大鼠肾脏组织AQP2表达、mRNA和蛋白的相对表达量(分别为0.2013±0.0417、0.98±0.33和0.94±0.21,n=13)均显著高于对照组(分别为0.1518 ±0.0214、0.58 ±0.51和0.51 ±0.46,n=20)(P均＜0.05),而培哚普利组心衰亚组大鼠(分别为0.0712 ±0.0218、0.76 ±0.45和0.82±0.49,n=13)均显著低于生理盐水组心衰亚组,但仍高于对照组(P均＜0.05).生理盐水组心衰亚组大鼠血浆AVP浓度、尿液AQP2浓度[分别为(82.52±11.77) ng/L、(19.72 ±3.91) ng/ml,n=13]均显著高于对照组[分别为(51.67±12.58) ng/L、(6.94±3.10)ng/ml,n=20](P均＜0.05),培哚普利组心衰亚组大鼠[分别为(15.65 ±4.10) ng/L、(71.65 ±9.21) ng/ml,n=13]均显著低于生理盐水组心衰亚组,但仍显著高于对照组(P均＜0.05).结论 慢性心力衰竭大鼠肾脏AQP2表达水平及尿液AQP2排泄均升高,而培哚普利可下调AQP2的表达水平、减少尿液AQP2排泄.
目的 探討慢性心力衰竭(心衰)大鼠腎髒水通道蛋白2(aquaporin-2,AQP2)錶達和尿液AQP2濃度的變化,及培哚普利對其的影響.方法 雄性SD大鼠60隻,按照簡單隨機化分組法分為對照組、生理鹽水組和培哚普利組,每組20隻.建立大鼠心衰模型,生理鹽水組、培哚普利組大鼠左心室梗死麵積(left ventricular myocardial infarction size,LVMI)≥20％者選入各自心衰亞組,LVMI＜20％者選入各自心功能代償亞組.榦預後檢測大鼠血壓、血鈉濃度、尿量以及尿滲透壓,免疫組織化學、逆轉錄-聚閤酶鏈反應(RT-PCR)、蛋白質印跡法(Western blot)法檢測大鼠腎髒AQP2 mRNA和蛋白的錶達情況,放射免疫法檢測血漿血管加壓素(arginine vasopressin,AVP)的濃度,間接ELISA法檢測尿液AQP2的濃度.結果 生理鹽水組心衰亞組大鼠腎髒組織AQP2錶達、mRNA和蛋白的相對錶達量(分彆為0.2013±0.0417、0.98±0.33和0.94±0.21,n=13)均顯著高于對照組(分彆為0.1518 ±0.0214、0.58 ±0.51和0.51 ±0.46,n=20)(P均＜0.05),而培哚普利組心衰亞組大鼠(分彆為0.0712 ±0.0218、0.76 ±0.45和0.82±0.49,n=13)均顯著低于生理鹽水組心衰亞組,但仍高于對照組(P均＜0.05).生理鹽水組心衰亞組大鼠血漿AVP濃度、尿液AQP2濃度[分彆為(82.52±11.77) ng/L、(19.72 ±3.91) ng/ml,n=13]均顯著高于對照組[分彆為(51.67±12.58) ng/L、(6.94±3.10)ng/ml,n=20](P均＜0.05),培哚普利組心衰亞組大鼠[分彆為(15.65 ±4.10) ng/L、(71.65 ±9.21) ng/ml,n=13]均顯著低于生理鹽水組心衰亞組,但仍顯著高于對照組(P均＜0.05).結論 慢性心力衰竭大鼠腎髒AQP2錶達水平及尿液AQP2排洩均升高,而培哚普利可下調AQP2的錶達水平、減少尿液AQP2排洩.
목적 탐토만성심력쇠갈(심쇠)대서신장수통도단백2(aquaporin-2,AQP2)표체화뇨액AQP2농도적변화,급배타보리대기적영향.방법 웅성SD대서60지,안조간단수궤화분조법분위대조조、생리염수조화배타보리조,매조20지.건립대서심쇠모형,생리염수조、배타보리조대서좌심실경사면적(left ventricular myocardial infarction size,LVMI)≥20％자선입각자심쇠아조,LVMI＜20％자선입각자심공능대상아조.간예후검측대서혈압、혈납농도、뇨량이급뇨삼투압,면역조직화학、역전록-취합매련반응(RT-PCR)、단백질인적법(Western blot)법검측대서신장AQP2 mRNA화단백적표체정황,방사면역법검측혈장혈관가압소(arginine vasopressin,AVP)적농도,간접ELISA법검측뇨액AQP2적농도.결과 생리염수조심쇠아조대서신장조직AQP2표체、mRNA화단백적상대표체량(분별위0.2013±0.0417、0.98±0.33화0.94±0.21,n=13)균현저고우대조조(분별위0.1518 ±0.0214、0.58 ±0.51화0.51 ±0.46,n=20)(P균＜0.05),이배타보리조심쇠아조대서(분별위0.0712 ±0.0218、0.76 ±0.45화0.82±0.49,n=13)균현저저우생리염수조심쇠아조,단잉고우대조조(P균＜0.05).생리염수조심쇠아조대서혈장AVP농도、뇨액AQP2농도[분별위(82.52±11.77) ng/L、(19.72 ±3.91) ng/ml,n=13]균현저고우대조조[분별위(51.67±12.58) ng/L、(6.94±3.10)ng/ml,n=20](P균＜0.05),배타보리조심쇠아조대서[분별위(15.65 ±4.10) ng/L、(71.65 ±9.21) ng/ml,n=13]균현저저우생리염수조심쇠아조,단잉현저고우대조조(P균＜0.05).결론 만성심력쇠갈대서신장AQP2표체수평급뇨액AQP2배설균승고,이배타보리가하조AQP2적표체수평、감소뇨액AQP2배설.
Objective To determine the expression of kidney aquaporin-2 (AQP2) and urine AQP2 excretion in chronic heart failure (CHF) rats and investigate effects of perindopril on the expression and excretion of AQP2.Methods Sixty rats were randomized into three groups:control group,CHF group,CHF + Perindopril group.According to left ventricular myocardial infarction size,CHF group and perindopril group were further divided into heart failure subgroup (LVMI ≥ 20％)and cardiac functional compensation subgroup(LVMI ＜ 20％),respectively.Blood and urine samples were collected from the rats for measuring serum Na+,urine volume and urine osmolality.The concentration of plasma arginine vasopressin (p-AVP) was detected by radioimmunoassay (RIA).Immunohistochemistry,semi-quantitative real time-polymerase chain reaction (RT-PCR) and Western blot were performed for measurement of kidney inner medullary AQP2.The concentration of Urine AQP2 was measured by indirect enzyme-linked immunosorbent assay (indirect ELISA).Results Immunohistochemistry,RT-PCR,Western blot examinations revealed increased quantity of the inner kidney medullary AQP2 expression (0.2013 ± 0.0417),AQP2 mRNA (0.98 ± 0.33)and AQP2 protein expression(0.94 ± 0.21) in heart failure subgroup (n =13) compared to control group (n =20,0.1518 ±0.0214,0.58 ±0.51,0.51 ±0.46),which could be significantly by perindopril(n =13,0.0712 ±0.0218,0.76 ±0.45,0.82 ±0.49,all P ＜0.05 vs.heart failure subgroup).The concentration of plasma arginine AVP[(19.72 ±3.91) ng/ml] and Urine AQP2[(82.52 ± 11.77) ng/L] were significantly higher in heart failure subgroup than in control group [n =20,(51.67 ± 12.58) ng/L,(6.94 ± 3.10)ng/ml] (P ＜ 0.05),which were significantly reduced by perindopril [n =13,(15.65 ± 4.10) ng/L,(71.65 ±9.21) ng/ml].Conclusion Increased expression of the kidney inner medullary AQP2 and the excretion of urine AQP2 in chronic heart failure rats could be reduced by perindopril.
