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目的：了解基础状态动物模型肾局部ＲＡＳ的水平，观察其在用转换酶抑制剂（ＡＣＥＩ）和血管紧张素受体拮抗剂（ＡＴ１ＲＡ）干预治疗后的变化，探讨、比较这两种药物对肾保护作用的分子生物学机制。方法：用反转录聚合酶链反应（ＲＴ－ＰＣＲ）， 分别对自发性高血压大鼠（ＳＨＲ）肾皮质内ＡＣＥ和ＡＴ１ 受体ｍ ＲＮＡ表达进行测定，观察用ＡＣＥＩ或ＡＴ１ＲＡ干预治疗后的变化。结果：（１）与ＷＫＹ比，基础状态下ＳＨＲ肾皮质内ＡＣＥ和ＡＴ１受体ｍ ＲＮＡ表达均显著升高（两组Ｐ＜ ０．０５）；（２）与对照组相比，用ＡＣＥＩ后ＳＨＲ 肾皮质内ＡＣＥｍ ＲＮＡ 被抑制（Ｐ＜ ０．０５），但ＡＴ１ 受体ｍ ＲＮＡ无变化；（３）与对照组相比，用ＡＴ１ＲＡ后，ＳＨＲ肾皮质内ＡＣＥ和ＡＴ１ 受体ｍ ＲＮＡ均被抑制（两组Ｐ＜ ０．０５）。结论：ＡＣＥＩ和ＡＴ１ＲＡ 都对ＳＨＲ局部ＲＡＳ有作用，但作用机理和途径可能不同，ＡＴ１ 受体可能存在多方面调节机制。ＡＣＥＩ似乎仅作用于ＡＣＥ，对ＡＴ１ 受体可能没有直接作用；ＡＴ１ＲＡ在作用于ＡＴ１ 受体的同时，可能还通过旁路途径作用于ＡＣＥ
OBJECTIVE: To investigate the changes of renal local RAS in animal model of basal state and to observe its changes after interventional treatment with ACEI and AT1RA, and to compare the effects of these two drugs on kidney Molecular biology of protection. Methods: The expression of ACE and AT1 receptor mRNA in the renal cortex of spontaneously hypertensive rats (SHR) were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). The effects of ACEI or AT1RA intervention were observed Variety. Results: (1) Compared with WKY, the expression of ACE and AT1 receptor m RNA in renal cortex of SHR were significantly increased (P <0.05); (2) Compared with control group, ACE mRNA in the renal cortex of SHR was inhibited (P <0.05), but there was no change in the m RNA of AT1 receptor. (3) Compared with the control group, both ACE and AT1 receptor m RNA Was suppressed (P <0.05 for both groups). CONCLUSION: ACEI and AT1RA both have effects on local RAS in SHR, but their mechanism and pathway may be different. There may be many regulatory mechanisms of AT1 receptor. ACEI seems to act only on ACE and may not have a direct effect on AT1 receptors; while AT1RA may act on AT1 receptors at the same time as ACEs via the alternative pathway