Renal Artery Stenosis (RAS) is the narrowing of renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. Possible complications of renal artery stenosis are renovascular hypertension and renal ischemia. The goals of the current study were to investigate the physiological response to RAS and effects of the artery and stenosis geometry, quantify the performance of arterial pressure regulation mechanisms respect to stenosis severity, and predict future conditions of renal artery stenosis. Commercial software based on the finite volume method was utilized to solve governing equations. To determine the physiological response, simulations were done for two cases, with and without the involvement of arterial pressure regulation mechanisms. The numerical method was validated by experimental data, which obtained from two prototypes. Results showed that systemic blood pressure was increased as the physiological response to RAS; hence, the flow rate of the renal branch was improved and renal ischemia was relatively prevented. Furthermore, results demonstrated that the stenosis percentage and artery diameter were dominant geometric parameters on the hemodynamics and other parameters had negligible effects. It was demonstrated that 50% of stenosis was the critical point for the interaction of RAS and arterial pressure regulation mechanisms. Finally, wall shear stress was analyzed on an image-based geometry, and it was estimated and expected that acute renal artery stenosis was progressive and pathogenesis of arterial diseases.

肾动脉狭窄（RAS）是肾动脉狭窄，最常见的原因是动脉粥样硬化或纤维肌增生异常。肾动脉狭窄的可能并发症是肾血管性高血压和肾缺血。当前研究的目的是研究对RAS的生理反应以及动脉和狭窄几何形状的影响，量化关于狭窄严重程度的动脉压调节机制的性能，并预测肾动脉狭窄的未来状况。利用基于有限体积法的商业软件求解控制方程。为了确定生理反应，在有和没有动脉血压调节机制的情况下，对两种情况进行了模拟。数值方法通过从两个原型获得的实验数据进行了验证。结果表明，随着对RAS的生理反应，全身血压升高。因此，改善了肾分支的流速，并相对防止了肾脏缺血。此外，结果表明狭窄百分比和动脉直径是影响血液动力学的主要几何参数，其他参数的影响可忽略不计。结果表明，狭窄的50％是RAS与动脉压调节机制相互作用的关键点。最后，在基于图像的几何结构上分析了壁切应力，并估计并预期急性肾动脉狭窄是进行性疾病和动脉疾病的发病机制。改善了肾分支的流速，相对预防了肾脏缺血。此外，结果表明狭窄百分比和动脉直径是影响血液动力学的主要几何参数，其他参数的影响可忽略不计。结果表明，狭窄的50％是RAS与动脉压调节机制相互作用的关键点。最后，在基于图像的几何结构上分析了壁切应力，并估计并预期急性肾动脉狭窄是进行性疾病和动脉疾病的发病机制。改善了肾分支的流速，相对预防了肾脏缺血。此外，结果表明狭窄百分比和动脉直径是影响血液动力学的主要几何参数，其他参数的影响可忽略不计。结果表明，狭窄的50％是RAS与动脉压调节机制相互作用的关键点。最后，在基于图像的几何结构上分析了壁切应力，并估计并预期急性肾动脉狭窄是进行性疾病和动脉疾病的发病机制。结果表明，狭窄的50％是RAS与动脉压调节机制相互作用的关键点。最后，在基于图像的几何结构上分析了壁切应力，并估计并预期急性肾动脉狭窄是进行性疾病和动脉疾病的发病机制。结果表明，狭窄的50％是RAS与动脉压调节机制相互作用的关键点。最后，在基于图像的几何结构上分析了壁切应力，并估计并预期急性肾动脉狭窄是进行性疾病和动脉疾病的发病机制。