scholarly journals Role of the epithelial sodium channel in salt-sensitive hypertension

2011 ◽  
Vol 32 (6) ◽  
pp. 789-797 ◽  
Author(s):  
Yan Sun ◽  
Jia-ning Zhang ◽  
Dan Zhao ◽  
Qiu-shi Wang ◽  
Yu-chun Gu ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Salt Sensitive Hypertension

scholarly journals Epithelial Sodium Channel and Salt-Sensitive Hypertension

Hypertension ◽  
2021 ◽  
Vol 77 (3) ◽  
pp. 759-767
Author(s):  
Stephanie M. Mutchler ◽  
Annet Kirabo ◽  
Thomas R. Kleyman
Keyword(s):  
Blood Pressure ◽  
Sodium Channel ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Pressure Rise ◽  
Epithelial Sodium Channel ◽  
Sodium Reabsorption ◽  
High Salt Intake ◽  
Salt Sensitive Hypertension

The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.

scholarly journals Role of the epithelial sodium channel (ENaC) in the development of salt‐sensitive hypertension

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Tengis S. Pavlov ◽  
Vladislav Levchenko ◽  
Daria V. Ilatovskaya ◽  
Paul M. O'Connor ◽  
Allen W. Cowley ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Salt Sensitive Hypertension ◽  
Epithelial Sodium Channel Enac

Role of the α-, β-, and γ-Subunits of Epithelial Sodium Channel in a Model of Polygenic Hypertension

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Reinhold Kreutz ◽  
Berthold Struk ◽  
Speranza Rubattu ◽  
Norbert Hübner ◽  
Josiane Szpirer ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel

Role of SGK in hormonal regulation of epithelial sodium channel in A6 cells

2003 ◽  
Vol 284 (2) ◽  
pp. C404-C414 ◽  
Author(s):  
Diego Alvarez de la Rosa ◽  
Cecilia M. Canessa
Keyword(s):  
Sodium Channel ◽  
Hormonal Regulation ◽  
Apical Membrane ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Epithelial Sodium Channel ◽  
Hormonal Stimulation ◽  
A6 Cells ◽  
Epithelial Sodium Channel Enac

The purpose of this study was to examine the role of the serum- and glucocorticoid-induced kinase (SGK) in the activation of the epithelial sodium channel (ENaC) by aldosterone, arginine vasopressin (AVP), and insulin. We used a tetracycline-inducible system to control the expression of wild-type (SGK[Formula: see text]), constitutively active (S425D mutation; SGK[Formula: see text]), or inactive (K130M mutation; SGK[Formula: see text]) SGK in A6 cells independently of hormonal stimulation. The effect of SGK expression on ENaC activity was monitored by measuring transepithelial amiloride-sensitive short-circuit current ( I sc) of transfected A6 cell lines. Expression of SGK[Formula: see text] or SGK[Formula: see text] and aldosterone stimulation have additive effects on I sc. Although SGK could play some role in the aldosterone response, our results suggest that other mechanisms take place. SGK[Formula: see text] abrogates the responses to AVP and insulin; hence, in the signaling pathways of these hormones there is a shared step that is stimulated by SGK. Because AVP and insulin induce fusion of vesicles to the apical membrane, our results support the notion that SGK promotes incorporation of channels in the apical membrane.

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