Journal
HYPERTENSION
Volume 77, Issue 3, Pages 759-767Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.120.14481
Keywords
blood pressure; endothelium; extracellular fluid; nephrons; smooth muscle; sodium
Categories
Funding
- National Institutes of Health [R01 HL147818, K01 HL130497, P30 DK079307, T32 DK007052]
- Relypsa, Inc.
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The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. There is a spectrum of sodium-sensitivity among individuals, partly due to genetic variation in pathways involved in sodium handling and excretion. ENaC plays a crucial role in regulating extracellular fluid volume and blood pressure by facilitating sodium reabsorption in the distal nephron.
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.
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