逼尿肌过度活动（Detrusor overactivity, DO)是目前膀胱功能疾病中的研究热点。目前研究发现，逼尿肌细胞兴奋性异常是DO发生的重要机制，而钙离子失衡在其中发挥关键作用。文献及我们发现，钠钙交换体（NCX）是调节细胞内钙平衡的重要通道，在膀胱兴奋调控中发挥作用。在大鼠DO预实验中，我们发现NCX1表达显著增高，产生了类似DO的异常收缩。结合文献及实验基础，我们推测NCX1通过控制逼尿肌细胞内的钙离子，引发了逼尿肌细胞兴奋性异常，在大鼠DO中发挥重要作用，并可能受上游ROS/HIF-1α的调控。本课题拟用大鼠膀胱出口部分梗阻模型，通过钙负载、膜片钳、实时定量PCR等技术，验证NCX1在大鼠DO中的作用，进一步通过基因沉默、免疫共沉淀等技术，探索ROS是否通过HIF-1α调控NCX1的作用机制。对阐明DO的发生及发展，有重要意义，为预防和治疗DO提供新的理论和作用靶点。

Detrusor overactivity (DO) which is a research hotspot in the diseases of bladder function. At present, more and more evidence indicated that the spontaneous of detrusor cell was an important mechanism of DO, and calcium ions imbalance played a key role in the regulation of detrusor excitability. Previous reports and our studies have found, the sodium calcium exchanger (NCX) is an important channel to regulate intracellular calcium, play an important role in bladder excitation regulation. In the pre experiment of rat after PBOO, we found that NCX1 expression was significantly increased, stimulated the NCX1 induced abnormal contraction similar to DO. Combined with the past studies, we speculate that NCX1 by controlling the intracelluar of calcium in the detrusor cells, triggered the detrusor excitability abnormality, play an important role in the regulation of DO in rats, and may be affected by the upstream ROS/HIF-1α. This topic with a rat after PBOO to simulate the detrusor overactivity, the calcium measurement, patch clamp, real-time quantitative PCR, verified the function of NCX1 in rat DO. Then, used the gene silencing, CO immunoprecipitation technique to investigate the regulation of NCX1 by ROS/HIF-1α. To elucidate the mechanism and regulation of DO could provide new theory and targets for the prevention and treatment of DO.