交感神经活性增加对靶器官的损害可以独立于高血压而单独存在[1]。对于肾脏而言,交感神经传出活性增加导致肾血流量减少、肾素释放、水钠潴留;交感神经传入大脑活性增加则刺激中枢交感,导致神经源性高血压[2]。因此,降低肾脏交感神经活性,对于治疗高血压在理论上是可行的。基于此理论,早在20世纪30年代,神经外科专家就已经开始尝试切除肾脏交感神经来治疗高血压。当然,在那个年代,肾交感神经切 Sympathetic nerve activity of the target organ damage can be independent of hypertension and exist alone [1]. For the kidneys, increased sympathetic outflow leads to decreased renal blood flow, renin release, sodium retention; increased sympathetic afferent activity in the brain stimulates central sympathetic responses and leads to neurogenic hypertension [2]. Therefore, reducing renal sympathetic activity is theoretically feasible for the treatment of hypertension. Based on this theory, as early as the 1930s, neurosurgeons began to try to remove the renal sympathetic nerve to treat hypertension. Of course, in those days, the kidneys were sympathetically cut