论文部分内容阅读
目的：观察氯沙坦对自发性高血压大鼠（ＳＨＲ）血浆、左室及主动脉组织中血管紧张素Ⅱ（ＡｎｇⅡ）水平的影响，并探讨其降压和逆转心血管肥厚的作用与心血管局部组织中ＡｎｇⅡ的关系。方法：将１６ 周龄的ＳＨＲ随机分成ＳＨＲ－Ｌ（氯沙坦治疗）组与ＳＨＲ－Ｃ（非治疗对照）组，另设同源正常血压大鼠ＷＫＹ组。饲养时间共六周。大鼠的收缩压和心率用尾套法测量，实验前及实验开始后每两周测一次。左室重量指数（ＬＶⅠ）及主动脉中膜与内径比率在第六周实验结束前测量。血浆、心肌和主动脉ＡｎｇⅡ含量用放免法测量。以ＳＨＲ－Ｃ组做直线相关分析。结果：氯沙坦能显著降低ＳＨＲ的收缩压，在４ 周后降至最低水平，对心率无影响。ＳＨＲ－Ｌ与ＳＨＲ－Ｃ组比较ＬＶⅠ及主动脉中膜与内径比值下降，但未降至ＷＫＹ水平。左室及主动脉ＡｎｇⅡＳＨＲ－Ｃ组高于ＷＫＹ组，且分别与ＬＶⅠ及主动脉中膜与内径比值呈正相关。ＳＨＬ－Ｌ组ＡｎｇⅡ水平均高于ＳＨＲ－Ｃ组，且以血浆升高最明显。结论：ＳＨＲ左室及主动脉组织中ＡｎｇⅡ升高是造成左室及主动脉肥厚的重要因素。氯沙坦通过阻断ＡＴ１受体产生降压及逆转心血管肥厚的作用
Objective: To observe the effect of losartan on the level of angiotensin Ⅱ (Ang Ⅱ) in plasma, left ventricle and aorta of spontaneously hypertensive rats (SHR) and to explore its antihypertensive effects and its role in reversing cardiovascular hypertrophy Relationship between angiotensin II and angiotensin Ⅱ in vascular tissue. Methods: 16-week-old SHRs were randomly divided into SHR-L (losartan-treated) group and SHR-C (untreated control) group, and another WKY group with normal normotensive rats. Feeding time for a total of six weeks. Systolic pressure and heart rate in rats were measured by tail cuff method, and the test was performed every two weeks before the experiment and after the start of the experiment. Left ventricular mass index (LVI) and aortic medial to medial diameter ratio were measured at the end of the sixth week of the experiment. Ang Ⅱ levels in plasma, myocardium and aorta were measured by radioimmunoassay. Linear correlation analysis was done with SHR-C group. Losartan significantly reduced the systolic blood pressure of SHR and reached its lowest level after 4 weeks, with no effect on heart rate. Compared with SHR-C and SHR-C groups, the ratio of LVⅠ and aorta middle membrane decreased but did not decrease to WKY level. The left ventricular and aortic AngⅡSHR-C group was higher than the WKY group, and were positively correlated with the ratio of LV Ⅰ and aorta medial membrane to the diameter. The level of Ang Ⅱ in SHL-L group was higher than that in SHR-C group, and the most obvious increase was in plasma. Conclusion: The increase of Ang II in left ventricular and aorta of SHR is an important factor of hypertrophy of left ventricle and aorta. Losartan blocks blood pressure and reverses cardiovascular hypertrophy by blocking AT1 receptors