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      Involvement of ENaC in the development of salt-sensitive hypertension

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          Abstract

          Salt-sensitive hypertension is associated with renal and vascular dysfunctions, which lead to impaired fluid excretion, increased cardiac output, and total peripheral resistance. It is commonly accepted that increased renal sodium handling and plasma volume expansion are necessary factors for the development of salt-induced hypertension. The epithelial sodium channel (ENaC) is a trimeric ion channel expressed in the distal nephron that plays a critical role in the regulation of sodium reabsorption in both normal and pathological conditions. In this mini-review, we summarize recent studies investigating the role of ENaC in the development of salt-sensitive hypertension. On the basis of experimental data obtained from the Dahl salt-sensitive rats, we and others have demonstrated that abnormal ENaC activation in response to a dietary NaCl load contributes to the development of high blood pressure in this model. The role of different humoral factors, such as the components of the renin-angiotensin-aldosterone system, members of the epidermal growth factors family, arginine vasopressin, and oxidative stress mediating the effects of dietary salt on ENaC are discussed in this review to highlight future research directions and to determine potential molecular targets for drug development.

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          Author and article information

          Journal
          Am J Physiol Renal Physiol
          Am. J. Physiol. Renal Physiol
          ajprenal
          ajprenal
          AJPRENAL
          American Journal of Physiology - Renal Physiology
          American Physiological Society (Bethesda, MD )
          1931-857X
          1522-1466
          1 August 2017
          21 December 2016
          1 August 2018
          : 313
          : 2
          : F135-F140
          Affiliations
          [1] 1Division of Hypertension and Vascular Research, Henry Ford Hospital , Detroit, Michigan; and
          [2] 2Department of Physiology, Medical College of Wisconsin , Milwaukee, Wisconsin
          Author notes
          Address for reprint requests and other correspondence: T. S. Pavlov, Div. of Hypertension and Vascular Research, Henry Ford Hospital, 2799 W. Grand Blvd., Detroit, MI 48202 (e-mail: tpavlov1@ 123456hfhs.org ).
          Author information
          http://orcid.org/0000-0002-6481-0390
          http://orcid.org/0000-0002-5190-8356
          Article
          PMC5582899 PMC5582899 5582899 F-00427-2016 F-00427-2016
          10.1152/ajprenal.00427.2016
          5582899
          28003189
          d92f80b1-5d6a-4c80-9557-e13f95f97b67
          Copyright © 2017 the American Physiological Society
          History
          : 2 August 2016
          : 20 December 2016
          : 20 December 2016
          Funding
          Funded by: http://doi.org/10.13039/100000050 HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)
          Award ID: HL116603
          Award ID: HL108880
          Award ID: HL122662
          Categories
          Review

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