CAJ | 학술논문

　　目的观察缬沙坦对自发性高血压大鼠（SHR）左心室心肌细胞G蛋白偶联受体激酶2（GRK2）的表达及亚细胞分布的影响。方法18只SHR随机分为对照组（n=6），低剂量缬沙坦组[SHRL组，10mg/（kg·d），n=6]和高剂量缬沙坦组[SHRH组，30mg/（kg·d），n=6]，由6月龄喂养至8月龄，处死后分离心脏，通过免疫荧光标记、激光共聚焦显微镜及Werstern blot方法，观察左心室心肌细胞GRK2的表达及亚细胞分布的变化。结果与对照组比较，SHRL组及SHRH组左心室心肌组织总蛋白、浆蛋白及膜蛋白GRK2表达水平有明显减少（P＜0.05），SHRH组较SHRL组减少更明显（P＜0.05）；与对照组比较， SHRL组及SHRH组GRK2在心肌细胞膜上分布减少，SHRH组较SHRL组进一步减少。结论缬沙坦能减少SHR左心室心肌细胞GRK2的表达及在细胞膜上的分布，这可能是逆转心肌肥大及心室重塑的机制之一。
　　목적관찰힐사탄대자발성고혈압대서（SHR）좌심실심기세포G단백우련수체격매2（GRK2）적표체급아세포분포적영향。방법18지SHR수궤분위대조조（n=6），저제량힐사탄조[SHRL조，10mg/（kg·d），n=6]화고제량힐사탄조[SHRH조，30mg/（kg·d），n=6]，유6월령위양지8월령，처사후분리심장，통과면역형광표기、격광공취초현미경급Werstern blot방법，관찰좌심실심기세포GRK2적표체급아세포분포적변화。결과여대조조비교，SHRL조급SHRH조좌심실심기조직총단백、장단백급막단백GRK2표체수평유명현감소（P＜0.05），SHRH조교SHRL조감소경명현（P＜0.05）；여대조조비교， SHRL조급SHRH조GRK2재심기세포막상분포감소，SHRH조교SHRL조진일보감소。결론힐사탄능감소SHR좌심실심기세포GRK2적표체급재세포막상적분포，저가능시역전심기비대급심실중소적궤제지일。
Objective To investigate the effects of valsartan on the expression and subcel ular distribution of G pro-tein- coupled receptor kinase 2(GRK2) in spontaneously hypertensive rat (SHR). Methods 18 six- month old SHRs were divided into control group (n=6), low- dose valsartan treatment group(SHRL group, n=6)and high- dose valsartan treatment group (SHRH group, n=6). Al rats feed to eight- month old and were sacrificed for heart isolation. The expression and sub-cel ular distribution of GRK2 in left ventricular myocardium were determined by immunofluorescent labeling, laser confocal microscope and western blotting. Results Compared with control group,the expression of GRK2 in total protein,cyto-plasmic protein and membrane protein of left ventricular myocardial tissue was significantly lower in SHRL group and SHRH group than in control group(P<0.05),and more significantly lower in SHRH group than in SHRL group(P<0.05). The distri-bution of GRK2 in myocardial cel membrane reduced significantly in SHRL and SHRH groups, which was more significant in SHRH group. Conclusion Valsartan reduces the expression and subcel ular distribution of GRK2 in myocardial cel membrane of SHR, which may be one of the mechanisms reversing cardiac hypertrophy.