肾脏钠代谢障碍是盐敏感性高血压形成的重要环节，细胞免疫在高血压的发生发展中有着重要作用。然而细胞免疫是否与盐敏感性高血压肾脏钠代谢障碍间存在联系尚未见报道。本课题在既往研究基础上，提出"盐敏感者体内免疫细胞比例失衡导致肾脏局部RAAS紊乱、钠代谢障碍是盐介导其血压升高重要环节"的假设，首先对盐敏感大鼠和免疫缺陷小鼠模型进行高盐及药物干预，研究免疫细胞在盐介导的血压升高、局部RAAS激活、钠通道转运等环节的影响；进一步在细胞水平上采用细胞共培养的方法探索免疫细胞自分泌RAAS能力及对肾小管细胞钠代谢通道的作用；最后既往建立的盐敏感人群队列中进行饮食干预，进一步验证免疫细胞平衡在盐敏感性高血压形成的关键地位。本研究探究细胞免疫与肾脏局部RAAS间的"对话"对肾脏钠代谢调节及靶器官损伤的作用，对阐明盐敏感性高血压的形成机制具有重要意义。

Renal sodium metabolism is an important link in the formation of salt sensitive hypertensive formation, Cellular immunity play the vital important role in the process of hypertension. However, the relationship between cellular immunity and renal sodium metabolism is still not clear. Based on our previous study, we put forward the hypothesis " the immune cells take part in salt sensitive through the imbalance of RAAS in kidney disorders ". Firstly, using the animal models of Dahl salt sensitive rat and knockout model mice, we explore the effect of immune cells in salt induced elevation of blood pressure and the assosication between immune cells and local RAAS system or SGK1-ENaC pathway through drug intervention; Then, the relationships would be confirmed in cell level; At last, we also would recuit the subjects of "the salt sensitive cohort", and maintained the dietary intervention, which would confirm the relationship between immune cells and the sodium metabolism dysfunction. We believe that this work would been of great significance to uncover the etiology of salt sensitive hypertension as well as to seek another drug targets for treatment of essential hypertension.