过氧亚硝基阴离子对肾功能的调节及其在盐敏感性高血压中的病理生理学意义
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  • 作者:Dewan ; S.A.Majid ; 练桂丽 ; 叶鹏
  • 关键词:过氧亚硝基阴离子 ; 肾脏保护 ; 盐敏感性高血压
  • 中文刊名:ZGGZ
  • 英文刊名:Chinese Journal of Hypertension
  • 机构:Department of Physiology,Tulane University School of Medicine,Tulane Hypertension & Renal Center of Excellence;
  • 出版日期:2017-11-15
  • 出版单位:中华高血压杂志
  • 年:2017
  • 期:v.25
  • 语种:中文;
  • 页:ZGGZ201711013
  • 页数:5
  • CN:11
  • ISSN:11-5540/R
  • 分类号:28-32
摘要
体内和体外研究显示,一氧化氮和超氧阴离子(O_2~-)相互作用,调节肾小管钠离子(Na~+)重吸收,以维持肾Na~+排泄。O_2~-与一氧化氮反应生成过氧亚硝基阴离子(ONOO~-),所以组织中O_2~-维持在最低水平。一般认为ONOO~-是体内一种与许多病理生理条件相关的氧化自由基。虽然已有研究阐明一氧化氮和O_2~-对肾小管的作用,但ONOO~-在调节肾小管Na~+重吸收中的特定作用尚不确定。已有研究证实,一氧化氮和O_2~-在生成ONOO~-过程中的相互作用对肾脏起重要保护作用,有助于在肾素血管紧张素系统激活的条件下,防止肾小管Na~+过度重吸收。然而,在病理生理条件下,特别是在盐敏感性高血压(SSH)中ONOO~-的调节作用尚不清楚。血管紧张素Ⅱ(AngⅡ)以及高盐摄入均可增加一氧化氮和O_2~-生成,促进ONOO~-产生。然而,在药理学抑制或基因缺失的情况下,一氧化氮合酶活性受损(解耦联),ONOO~-的形成减少。研究发现,与野生型小鼠相比,长期输注AngⅡ联合高盐摄入可导致内皮型一氧化氮合酶基因敲除小鼠(eNOSKO,一种ONOO~-生成最少的模型)发生严重高血压,加重肾损害,表明ONOO~-对输注AngⅡ所导致的这些不良反应起到保护作用。本综述全面讨论有关ONOO~-对肾脏功能的影响,旨在确定其在肾功能调节中的复杂相互作用,及其失衡是否与SSH的病理生理学相关。
        
引文
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