不同时期氯沙坦短暂治疗对自发性高血压大鼠心脏AT1受体、AT2受体表达的影响

目的 观察不同时期氯沙坦短暂治疗对自发性高血压大鼠(SHR)的血压变化及心脏AT1受体、AT2受体表达的影响,探讨血管紧张素Ⅱ 1型受体(AT1R)、血管紧张素Ⅱ2型受体(AT2R)在高血压发病机制中的作用,为早预防、早治疗高血压开辟新的途径.方法 选用4周龄SHR及京都Wistar大鼠(WKY),分成4组:氯沙坦4周...

Effect of transient treatment with losartan during different periods on the expression of cardiac AT1 receptor and AT2 receptor In spontaneously hypertensive rats

Objective To investigate the effect of transient treatment with losartan during different periods on blood pressure and the expression of cardiac AT1 receptor（AT1R） and AT2 receptor（ATe） in spontaneously hypertensive rats （SHR）. Methods Four-week-old male SHits were randomly treated with losartan from fourweek-old （SHR-Los4： Four-week-old SHR treated with losartan for 4 weeks and followed up until 24 weeks of age after drug cessation, n=8）, from 12 weeks（SHR-Losl2： 12-week-old SHR treated with losartan for 4 weeks and followed up until 24 weeks of age, n=8）, weekage-and sex-matched SHR （SHR） and Wistar Kyoto（WKY） rats were served as normal control （n=8 respective） and treated with saline. Left ventricular mass index （LVMI） was calculated by left ventricle weight/body weight. Cardiac AT1R and AT2R protein levels were examined by immunohistochemlcal method and the mRNA expression of AT1R and AT2R was semiquantified by RT-PCR. Resdts After treated with losartan for four weeks, SBP of SHR-Los4 during prehypertension was persistently reduced, and lower signitieanfly than SHR until age 24 weeks. SBP of SHR-Losl2 during hypertension rise rapidly, and was no difference compared to untreated SHR. LVMI in both SHR-Los4 and SHR-Losl2 was continuously decreased, and the protein and mRNA levels of cardiac ATIR were reduced persistently in groups with losartan treatment. Compared to untreated SHR, cardiac AT2R protein and mRNA levels in two groups with losartan were up-regulated, whereas no significant difference. Conclusion Treatment with losartan during different periods could lower blood pressure continuously, which might be achieved by long-term inhibition of renin-angiotensin systems.