对比剂急性肾损伤（CIAKI）是使用碘对比剂的重要并发症，但机制并不明确。对比剂在肾脏主要引起以血管活性物质失衡、血管收缩为特征的血流动力学改变和以肾小管上皮细胞凋亡为特征的细胞损伤。内质网应激(ERS)是诱导细胞凋亡的重要途径，而血管紧张素II是ERS的重要诱导因子。我们前期研究显示，血管紧张素转换酶抑制剂降低CIAKI的发生，提示血管紧张素II在CIAKI中起重要的作用。因此我们假设对比剂暴露通过激活肾素-血管紧张素系统，血管紧张素II活性增加，通过诱导ERS，导致肾小管上皮细胞凋亡。本研究拟通过用对比剂刺激肾小管上皮细胞及Wistar大鼠，检测血管紧张素II以及内质网应激和细胞凋亡相关的指标，并分别用阻断血管紧张素II受体阻断剂和ERS阻断剂进行干预，从体外细胞及动物体内试验水平评价血管紧张素II诱导ERS在CIAKI的作用及机制，为CIAKI发病机制及制定临床干预策略提供证据。

Contrast-induced acute kidney injury (CIAKI) is an important complication in the use of iodinated contrast media. The mechanism of developing CIAKI is not completely elucidated. Exposure to contrast media leads to renal hemodynamics changes due to unbalaced vaso-active substances and renal vessels constriction, and leads to damaged tubular epithelial cells attributed to apoptosis.Endoplasmic reticulum stress (ERS) appears to play an important role in cell apoptosis. And it is verified that angiotensin II is an important inducer of ERS. The result of our prevous study showed that angiotensin converting enzyme inhibitor might reduce the risk of CIAKI, thus indicated angiotensin II may play an important role in the development of CIAKI. Therefore, we proposed the hypothesis that the exposure to contrast media may activate RAAS to increase the level of angiotensin II, and that angiotensin II may induce ERS resulting in tubular epithelial cells apoptosis. In the study proposed, human renal proximal tubular cells (HK-2 cells) and Wistar rats were exposured to contrast media, paralleled with the angiotensin II type 1 receptor antagonist (Valsatan) or ERS inhibitor (tauroursodeoxycholic acid) to blocking the effects,respectively. The angiotensin II levels and ERS or apoptosis biomarkers were measured at a series of time points to evaluate the effect of ERS induced by angiotensin II on cell apoptosis after contrast media exposure. The results of our study will provide evidences for understanding the mechanism of CIAKI and formulating clinical preventive strategy.