摘要
目的:探讨培多普利对原发性高血压大鼠左心室肥厚重构及进程中血管紧张素II(Ang-II)和肌浆网钙ATP酶的影响。方法:原发性高血压大鼠分成模型组、培多普利治疗组[SHR-t1mg/(kg)·d],WKY大鼠为正常对照组(WKY)。电镜观察左心室肥厚的超微结构,并分别测定心肌指数(左室重/体质量,LV/WT),血、心肌Ang-II水平和肌浆网钙ATP酶的活性变化。结果:SHR-t组的血AngII水平无明显改变,SHR组的血压、LV/WT(3.98±0.32)mg/g、Ang-II(16.72±5.24)pg/mg水平显著升高(P<0.01),电镜下可见心肌相对缺氧及代偿性细胞功能活跃表现。SHR-t组血压、LV/WT(3.38±0.31)mg/g、Ang-II(12.94±1.63)pg/mg明显下降(P<0.05),且未见上述心肌超微结构改变;但SHR-t组的LV/BW与WKY组(2.29±0.49)mg/g相比仍有显著差异(P<0.01);SHR组肌浆网钙ATP酶活性明显下调[0.52±0.11μmol/(g·min),P<0.05],治疗后恢复[0.82±0.11μmol/(g·min),P<0.05],但仍未达正常。结论:ACE-I主要通过抑制局部肾素-血管紧张素系统通路,对高血压大鼠左心室肥厚重构起了很好的逆转作用,但不可能完全阻断左心室肥厚的进程。
Objective： To evaluate the effects of perindopfil on the angiotensin Ⅱ （AngoⅡ） and sareoplasmic reticulum（SR） Ca^2＋ ATPase in the process of left ventricular hypertrophy in the spontaneously hypertensive rat. Methods： The hypertensive rats were divided into model group（SHR） and treated group SHR-t（receiving perindopfil 1 mg/kg per day）, Wistar-Kyoto rats were chosen as normal-controlled group. Electron microscope was used to study the myocardial ultrastructural changes. The level of AngⅡ in plasma and cardiac muscle, the myocardial indexes （left ventricle mass/weight total LV/WT） and the SR Ca^2＋ ATPase activity were determined in 3 groups. Results： The level of AngII in the plasma did not change significantly after treatment. The blood pressure, the level of Ang-Ⅱ （16.72 ＋ 5.24 pg/mg） in cardiac muscle and LV/WT （3.98＋0.32mg/g） ratio of the SHR group were higher than those of the normal-controlled group （AngⅡ 12.07 ＋ 2.33 pg/mg LV/WT 2.29 ＋ 0.49 mg/g） （P 〈 0.01 ）. The electron microscope showed relatively hypoxia in myocardium and compensatory active function. The blood pressure, the level of Ang-Ⅱ in cardiac mycles and left ventricular mass were reduced significanth in treated group. （P 〈 0.05）, but the LV/WT ratio （3.38±0.31 mg/g）was still significantly higher than that of WKY group（P 〈 0.01 ）. The ulltrastructual abnormalities of myocardial tissue described above was not found in SHR-treated group. The SR Ca^2＋ ATPase activity[0.52±0.11μmol/（g.min） ] was decreased in the SHR group（P 〈 0.05）, After the treatment using perindopril, the SR Ca^2＋ ATPase activity was increased in SHR-treated group [0.82 ± 0.22 μmol/（g·min）, P 〈 0.05 ]. Conclusion： The ACE-Ⅰ plays a key role in reversing cardiac remodeling of SHR, through inhibiting renin-angiotensin system pathway. But it can＇t absolutely prevent left ventricular hypertrophy in SHR.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2006年第1期33-35,46,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
江苏省卫生厅科技基金资助项目(SK200205)
