肾素原受体参与肾脏对体液与电解质的调节（英文）

(Pro)Renin Receptor as a Novel Mediator of Renal Handling of Fluid and Electrolytes

最初的研究发现肾素原受体(PRR)作为肾素与肾素原的特异性受体,参与对肾素-血管紧张素系统(RAS)活性的调节。然而,最新的证据揭示PRR功能的多样性,PRR可以发挥RAS依赖性与非依赖性的作用。PRR可以被furin或ADAM19切割,产生两个功能性片段,一是28 ku可溶性PRR受体(s PRR),另一个是M8.9,后者是vacuolar H+-ATPase的一个亚型,负责H+转运。近些年的研究证明,PRR参与了许多的生理与病理生理过程的调节。比如,PRR通过调节集合管水通道-2(AQP2)与髓袢升枝粗段(TAL)Na^+,K^+,Cl^-共转运蛋白(NKCC2)的调节而决定尿液浓缩功能;PRR通过介导局部醛固酮的产生而促进K+的排泄;肾脏PRR过度激活介导了血管紧张素II与果糖/高盐诱导的高血压。总之,PRR是肾脏生理与病理生理过程的新的调节因子。

（Pro）renin receptor（PRR）was organically identified as a specific receptor for prorenin and renin to regulate the activity of renin-angiotensin system（RAS）.Increasing evidence suggests that PRR plays a multitude functions in a RAS-dependent and independent manner.The extracellular domain of PRR is cleaved by furin or ADAM19 to produce a 28-ku soluble PRR（sPRR）while the intracellular domain,M8.9,is a subunit of vacuolar H＋-ATPase that mediates H＋transport.PRR is critically involved in embryogenesis in low vertebrates and mammals.In recent years,a significant progress has been made in identifying the physiological and pathophysiological functions of renal PRR.PRR has been identified as an important regulator of urine concentrating capability mostly due to its ability to upregulate to aquaporin-2（AQP2）in the collecting duct and Na~＋,K~＋,2Cl^-cotransporter（NKCC2）in the thick ascending limb.PRR also promotes K~＋ secretion in response to K~＋ loading through extra-adrenal aldosterone（Aldo）production.Overactivation of renal PRR contributes to the pathogenesis of hypertension induced by angiotensin II infusion and fructose/salt.Overall,PRR has emerged as a new regulator of physiological and pathophysiological processes in the kidney.