PMID- 32852643
OWN - NLM
STAT- MEDLINE
DCOM- 20210311
LR  - 20210513
IS  - 1534-3111 (Electronic)
IS  - 1522-6417 (Print)
IS  - 1522-6417 (Linking)
VI  - 22
IP  - 9
DP  - 2020 Aug 27
TI  - ENaC in Salt-Sensitive Hypertension: Kidney and Beyond.
PG  - 69
LID - 10.1007/s11906-020-01067-9 [doi]
LID - 69
AB  - PURPOSE OF REVIEW: The main goal of this article is to discuss the role of the 
      epithelial sodium channel (ENaC) in extracellular fluid and blood pressure 
      regulation. RECENT FINDINGS: Besides its role in sodium handling in the kidney, 
      recent studies have found that ENaC expressed in other cells including immune 
      cells can influence blood pressure via extra-renal mechanisms. Dendritic cells 
      (DCs) are activated and contribute to salt-sensitive hypertension in an 
      ENaC-dependent manner. We discuss recent studies on how ENaC is regulated in both 
      the kidney and other sites including the vascular smooth muscles, endothelial 
      cells, and immune cells. We also discuss how this extra-renal ENaC can play a 
      role in salt-sensitive hypertension and its promise as a novel therapeutic 
      target. The role of ENaC in blood pressure regulation in the kidney has been well 
      studied. Recent human gene sequencing efforts have identified thousands of 
      variants among the genes encoding ENaC, and research efforts to determine if 
      these variants and their expression in extra-renal tissue play a role in 
      hypertension will advance our understanding of the pathogenesis of ENaC-mediated 
      cardiovascular disease and lead to novel therapeutic targets.
FAU - Pitzer, Ashley L
AU  - Pitzer AL
AD  - Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University 
      Medical Center, 2215 Garland Avenue, P415C Medical Research Building IV, 
      Nashville, TN, 37232, USA.
FAU - Van Beusecum, Justin P
AU  - Van Beusecum JP
AD  - Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University 
      Medical Center, 2215 Garland Avenue, P415C Medical Research Building IV, 
      Nashville, TN, 37232, USA.
FAU - Kleyman, Thomas R
AU  - Kleyman TR
AD  - Departments of Medicine, Cell Biology, Pharmacology, and Chemical Biology, 
      University of Pittsburgh, Pittsburgh, PA, USA.
FAU - Kirabo, Annet
AU  - Kirabo A
AD  - Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University 
      Medical Center, 2215 Garland Avenue, P415C Medical Research Building IV, 
      Nashville, TN, 37232, USA. annet.kirabo@vanderbilt.edu.
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University, 
      Nashville, TN, USA. annet.kirabo@vanderbilt.edu.
LA  - eng
GR  - P30 DK079307/DK/NIDDK NIH HHS/United States
GR  - F32 HL143927/HL/NHLBI NIH HHS/United States
GR  - R01 HL147818/HL/NHLBI NIH HHS/United States
GR  - F32 HL142237/HL/NHLBI NIH HHS/United States
GR  - T32 HL144446/HL/NHLBI NIH HHS/United States
GR  - K01 HL130497/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20200827
PL  - United States
TA  - Curr Hypertens Rep
JT  - Current hypertension reports
JID - 100888982
RN  - 0 (Epithelial Sodium Channels)
RN  - 0 (Sodium Chloride, Dietary)
SB  - IM
MH  - Blood Pressure
MH  - Endothelial Cells/metabolism
MH  - Epithelial Sodium Channels
MH  - Humans
MH  - *Hypertension
MH  - Kidney/metabolism
MH  - Sodium Chloride, Dietary/adverse effects/metabolism
PMC - PMC7452925
OTO - NOTNLM
OT  - ENaC
OT  - Hypertension
OT  - Inflammation
OT  - Sodium
COIS- The authors declare no conflicts of interest relevant to this manuscript.
EDAT- 2020/08/28 06:00
MHDA- 2021/03/12 06:00
PMCR- 2020/08/27
CRDT- 2020/08/28 06:00
PHST- 2020/08/28 06:00 [entrez]
PHST- 2020/08/28 06:00 [pubmed]
PHST- 2021/03/12 06:00 [medline]
PHST- 2020/08/27 00:00 [pmc-release]
AID - 10.1007/s11906-020-01067-9 [pii]
AID - 1067 [pii]
AID - 10.1007/s11906-020-01067-9 [doi]
PST - epublish
SO  - Curr Hypertens Rep. 2020 Aug 27;22(9):69. doi: 10.1007/s11906-020-01067-9.