PMID- 28724611
OWN - NLM
STAT- MEDLINE
DCOM- 20171017
LR  - 20220408
IS  - 1522-1466 (Electronic)
IS  - 1931-857X (Print)
IS  - 1522-1466 (Linking)
VI  - 313
IP  - 4
DP  - 2017 Oct 1
TI  - Tumor necrosis factor-alpha, kidney function, and hypertension.
PG  - F1005-F1008
LID - 10.1152/ajprenal.00535.2016 [doi]
AB  - Hypertension is considered to be a low-grade inflammatory condition characterized 
      by the presence of various proinflammatory cytokines. Tumor necrosis factor-alpha 
      (TNF-alpha) is a constituent of the proinflammatory cytokines that is associated with 
      salt-sensitive hypertension (SSH) and related renal injury. Elevated angiotensin 
      II (ANG II) and other factors such as oxidative stress conditions promote TNF-alpha 
      formation. Many recent studies have provided evidence that TNF-alpha exerts a direct 
      renal action by regulating hemodynamic and excretory function in the kidney. The 
      cytokine incites a strong natriuretic response and plays a part in regulation of 
      the intrarenal renin-angiotensin system. The exact mechanistic role of TNF-alpha in 
      the development of SSH is as yet poorly understood. While TNF-alpha antagonism has 
      been shown to attenuate hypertensive responses in many hypertensive animal 
      models, contrasting findings demonstrate that the direct systemic administration 
      of TNF-alpha usually induces hypotensive as well as natriuretic responses, indicating 
      a counterregulatory role of TNF-alpha in SSH. Differential activities of two cell 
      surface receptors of TNF-alpha (receptor type 1 and type 2) may explain the 
      contradictory functions of TNF-alpha in the setting of hypertension. This short 
      review will evaluate ongoing research studies that investigate the action of 
      TNF-alpha within the kidney and its role as an influential pathophysiological 
      variable in the development of SSH and renal injury. This information may help to 
      develop specific TNF-alpha receptor targeting as an effective treatment strategy in 
      this clinical condition.
CI  - Copyright (c) 2017 the American Physiological Society.
FAU - Mehaffey, Eamonn
AU  - Mehaffey E
AD  - Department of Physiology, Tulane Hypertension and Renal Center of Excellence, 
      Tulane University School of Medicine, New Orleans, Louisiana.
FAU - Majid, Dewan S A
AU  - Majid DSA
AD  - Department of Physiology, Tulane Hypertension and Renal Center of Excellence, 
      Tulane University School of Medicine, New Orleans, Louisiana majid@tulane.edu.
LA  - eng
GR  - P30 GM103337/GM/NIGMS NIH HHS/United States
GR  - R01 HL066432/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20170719
PL  - United States
TA  - Am J Physiol Renal Physiol
JT  - American journal of physiology. Renal physiology
JID - 100901990
RN  - 0 (Inflammation Mediators)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Sodium Chloride, Dietary)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - *Blood Pressure
MH  - Humans
MH  - Hypertension/immunology/*metabolism/physiopathology
MH  - Inflammation/immunology/*metabolism/physiopathology
MH  - Inflammation Mediators/immunology/*metabolism
MH  - Kidney/immunology/*metabolism/physiopathology
MH  - Receptors, Tumor Necrosis Factor, Type I/metabolism
MH  - Receptors, Tumor Necrosis Factor, Type II/metabolism
MH  - Renin-Angiotensin System
MH  - Signal Transduction
MH  - Sodium Chloride, Dietary/*adverse effects
MH  - Tumor Necrosis Factor-alpha/immunology/*metabolism
PMC - PMC5668589
OTO - NOTNLM
OT  - TNF-alpha
OT  - inflammatory cytokines
OT  - natriuresis
OT  - renin-angiotensin system
EDAT- 2017/07/21 06:00
MHDA- 2017/10/19 06:00
PMCR- 2018/10/01
CRDT- 2017/07/21 06:00
PHST- 2016/10/31 00:00 [received]
PHST- 2017/06/30 00:00 [revised]
PHST- 2017/07/15 00:00 [accepted]
PHST- 2017/07/21 06:00 [pubmed]
PHST- 2017/10/19 06:00 [medline]
PHST- 2017/07/21 06:00 [entrez]
PHST- 2018/10/01 00:00 [pmc-release]
AID - ajprenal.00535.2016 [pii]
AID - F-00535-2016 [pii]
AID - 10.1152/ajprenal.00535.2016 [doi]
PST - ppublish
SO  - Am J Physiol Renal Physiol. 2017 Oct 1;313(4):F1005-F1008. doi: 
      10.1152/ajprenal.00535.2016. Epub 2017 Jul 19.