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目的探讨卡托普利治疗自发性高血压大鼠（ＳＨＲ）对循环和局部肾素－血管紧张素系统（ＲＡＳ）的长期影响。方法雄性ＳＨＲ（ｎ＝４３）宫内期始，予卡托普利治疗（１００ｍｇ·ｋｇ－１·ｄ－１）到１６周，并分别在１６周（ｎ＝１９）和４０周（ｎ＝２４）处死，年龄、性别、数量配对的未治疗ＳＨＲ和Ｗｉｓｔａｒ－ｋｙｏｔｏ（ＷＫＹ）大鼠作对照。测定收缩压（ＳＢＰ）、左室重（ＬＶＭ）与体重（ＢＷ）比、左室心肌和血浆血管紧张素Ⅱ（ＡｎｇⅡ）浓度（放免测定法）、主动脉和血清血管紧张素转换酶（ＡＣＥ）活性（紫外分光光度法）、肾脏和肝脏血管紧张素原（ＡＧＴ）基因表达、肾脏肾素基因表达（ＮｏｒｔｈｅｒｎＢｌｏｔ）。结果卡托普利治疗显著降低ＳＨＲ１６周ＳＢＰ和ＬＶＭ／ＢＷ，并持续到４０周。治疗不影响ＢＷ、血浆ＡｎｇⅡ浓度、血清ＡＣＥ活性和肝脏ＡＧＴ基因表达，但明显减少ＳＨＲ４０周左室心肌ＡｎｇⅡ浓度，抑制ＳＨＲ１６周主动脉ＡＣＥ活性，并持续到４０周，减少ＳＨＲ１６周和４０周肾脏ＡＧＴ基因的表达，卡托普利治疗停药前肾脏肾素基因表达明显增强。结论长期卡托普利治疗ＳＨＲ，停药后长时间抑制组织的肾素－血管紧张素系统如心肌ＡｎｇⅡ生成、主动脉ＡＣＥ活?
Objective To investigate the long-term effects of captopril on circulatory and regional renin-angiotensin system (RAS) in spontaneously hypertensive rats (SHR). Methods Male SHRs (n = 43) were treated with captopril (100 mg · kg-1 · d-1) for 16 weeks at the endometrial phase and were administered intravitreally at 16 weeks (n = 19) and 40 weeks 24), untreated SHR and Wistar-kyoto (WKY) rats sacrificed, age, sex, and number paired. (SBP), ratio of left ventricular mass (LVM) to body weight (BW), left ventricular myocardial and plasma concentrations of angiotensin Ⅱ (radioimmunoassay), aortic and serum angiotensin converting enzyme ) Activity (UV spectrophotometry), kidney and liver angiotensinogen (AGT) gene expression, and kidney renin gene expression (NorthernBlot). Results Captopril treatment significantly reduced SBP and LVM / BW at 16 weeks of SHR and continued for up to 40 weeks. The treatment did not affect BW, plasma AngⅡ concentration, serum ACE activity and hepatic AGT gene expression, but significantly decreased left ventricular Ang Ⅱ concentration in SHR40 weeks, inhibiting ACE activity of SHR16 aorta for 40 weeks, reducing SHR 16 weeks and 40 weeks AGT gene expression, captopril treatment of renal renin gene expression was significantly increased. Conclusion Long-term captopril treatment of SHR, long-time withdrawal after stopping the renin-angiotensin system such as myocardial Ang Ⅱ generation, aortic ACE activity?