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Hypertension ; 77(3): 759-767, 2021 03 03.
Artigo em Inglês | MEDLINE | ID: mdl-33486988

RESUMO

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.


Assuntos
Pressão Sanguínea/fisiologia , Canais Epiteliais de Sódio/metabolismo , Hipertensão/fisiopatologia , Cloreto de Sódio na Dieta/metabolismo , Animais , Humanos , Hipertensão/etiologia , Hipertensão/metabolismo , Transporte de Íons , Rim/metabolismo , Modelos Biológicos , Néfrons/metabolismo , Cloreto de Sódio na Dieta/administração & dosagem , Cloreto de Sódio na Dieta/efeitos adversos
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