《国际循环》：肾动脉狭窄时组织损伤的机制：是什么？

    <International Circulation>:  What are the mechanisms of tissue injury in renal artery stenosis?

     Lerman教授：组织损伤的机制包括氧化应激增加，这可能是血管紧张素II激活所致。肾脏灌注压下降会导致肾素释放，随后产生的血管紧张素II会增加催化氧自由基生成的酶的水平，上述变化使得肾脏局部和系统循环中的氧化应激水平增加。此外，肾动脉狭窄时炎症反应也会增加，可能与肾缺血有关，也可能是继发于氧化应激和缺氧。缺氧是否会直接导致肾损伤，目前尚有争议，因为临床试验并未显示整个肾脏的氧供下降。但是，肾脏似乎有局部的斑片状缺氧，这提示肾损伤可能与缺血有关。目前看来，导致肾损伤的罪魁祸首主要是血管紧张素II，而血管紧张素II的激活最初是机体的一种保护性机制，目的是在肾脏灌注减少的情况下维持肾功能和升高血压。

    Prof. Lerman: The mechanisms appear to involve an increase in oxidative stress that may be the result of the activation of angiotensin II. Angiotensin II， which is released by renin due to the decrease in renal perfusion pressure， increases expression of enzymes that produce oxygen radicals and this causes an increase in oxidative stress. In addition， there is an increase in inflammation probably due to ischemia but this mechanism is secondary to oxidative stress and hypoxia. Whether hypoxia contributes directly to renal injury is still controversial because clinical trials have not shown that there is a decrease in oxygen supply to the kidney in a global way. However， there seems to be a regional lack of oxygen in the kidney so there may be a role for ischemia as well. It appears that one of the major culprits is angiotensin II， which is activated initially as a defense mechanism to preserve the function of the kidney and increase blood pressure because of the hypoperfusion of the kidney.