Shehata Marlene F
Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.
Int Arch Med. 2009 Sep 29;2(1):28. doi: 10.1186/1755-7682-2-28.
The epithelial sodium channel [ENaC] is critical for the maintenance of sodium balance, extracellular fluid volume and long term blood pressure control. Monogenic disorders causing ENaC hyperactivity have led to a severe form of hereditary hypertension in humans, known as Liddle's syndrome. Similarly, in animal models, ENaC hyperactivity has been well documented in kidneys of salt-sensitive [S] Dahl rats [a genetic model of salt-sensitive hypertension] versus their normotensive control [Dahl salt-resistant [R] rats]. The purpose of the present review is to highlight the differential regulation of ENaC in kidneys of Dahl S versus R rats. A systematic overview of the putative role of alternative splicing of the main alpha subunit of ENaC [alpha ENaC] in modulating ENaC expression in kidneys of Dahl rats will be discussed. Finally, a better understanding of the meaningful contribution of ENaC in the pathogenesis of salt-sensitive hypertension will be achieved upon completion of this review.
上皮钠通道[ENaC]对于维持钠平衡、细胞外液容量和长期血压控制至关重要。导致ENaC活性亢进的单基因疾病已在人类中引发了一种严重的遗传性高血压，即Liddle综合征。同样，在动物模型中，与正常血压对照[Dahl盐抵抗性[R]大鼠]相比，盐敏感性[S]Dahl大鼠（盐敏感性高血压的遗传模型）的肾脏中ENaC活性亢进已有充分记录。本综述的目的是强调Dahl S大鼠与R大鼠肾脏中ENaC的差异调节。将讨论ENaC主要α亚基[αENaC]的可变剪接在调节Dahl大鼠肾脏中ENaC表达方面的假定作用的系统概述。最后，完成本综述后将更好地理解ENaC在盐敏感性高血压发病机制中的重要作用。
