盐敏感高血压是由高盐摄入而引发的血压升高，其病理机制复杂。研究表明，炎症反应和血管内皮损伤是盐敏感性高血压发生发展的重要诱因。我们通过临床预实验发现血小板NHE1与盐敏感高血压密切相关。转录组数据分析显示盐敏感性高血压发生过程中，NHE1编码基因Slc9a1基因在多种组织中异常增高。Dahl盐敏感高血压大鼠高盐喂养后，血小板活化率增加、血小板NHE1表达及Ca2+浓度增加、炎症因子表达增多；NHE1抑制剂阻断了高盐诱导的血小板活化率增加。因此我们假设，高盐状态下异常增高的血小板NHE1诱导血小板异常活化，参与了内皮炎症和盐敏感高血压及靶器官损伤发展。本课题拟通过血小板特异性NHE1 基因敲除小鼠急性和慢性高盐喂养实验以及体外细胞实验，研究NHE1诱导血小板的活化参与内皮损伤、盐敏感高血压及其靶器官损伤的作用机制，从而为盐敏感高血压及靶器官损伤的防治提供新的理论和临床依据。

Salt-sensitive Hypertension is characterized by greater rise in blood pressure (BP) after salt loading with complex pathological mechanism. It has been found that inflammation and endothelial injury are important factors causing salt-sensitive hypertension. Preliminary Clinical trials shows that platelet NHE1 closely related with salt-sensitive hypertension. Transcription omics data analysis shows that the NHE1, encoded by SLC9A1, expression was significant increase in several organs during salt-sensitive hypertension. Our pilot study found that Dahl salt-sensitive rat with high salt intake have increased platelet activation, membrane NHE1 expression, intracellular Ca2+concentration, and inflammatory factors expression. NHE1 inhibitor blocked the increased platelet activation via In Vitro study. Therefore we hypothesize that high salt intake develops salt-sensitive hypertension and organ injury via endothelial inflammation caused by abnormal NHE1 activating platelet. In this study, we use platelet specific NHE1 knock out mice(Conditional NHE1-/-) high salt intake experiment (acute and chronic) and In Vitro study by using platelet cell will be performed to further confirm the hypothesis. This study is supposed to find a novel mechanism and provide important reference for treatment and prevention of salt-sensitive hypertension and target organ damage.