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Am J Physiol Renal Physiol. 2017 Aug 1;313(2):F141-F144. doi: 10.1152/ajprenal.00465.2016. Epub 2017 Apr 12.

Inflammatory cytokines regulate renal sodium transporters: how, where, and why?

Author information

1
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville Tennesee; and.
2
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville Tennesee; and meena.madhur@vanderbilt.edu.
3
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Abstract

Hypertension is growing in epidemic proportions worldwide and is now the leading preventable cause of premature death. For over a century, we have known that the kidney plays a critical role in blood pressure regulation. Specifically, abnormalities in renal sodium transport appear to be a final common pathway that gives rise to elevated blood pressure regardless of the nature of the initial hypertensive stimulus. However, it is only in the past decade that we have come to realize that inflammatory cytokines secreted by innate and adaptive immune cells, as well as renal epithelial cells, can modulate the expression and activity of sodium transporters all along the nephron, leading to alterations in pressure natriuresis, sodium and water balance, and ultimately hypertension. This mini-review highlights specific cytokines and the transporters that they regulate and discusses why inflammatory cytokines may have evolved to serve this function.

KEYWORDS:

angiotensinogen; interferon-γ; interleukin-17; interleukin-6

PMID:
28404590
PMCID:
PMC5582911
DOI:
10.1152/ajprenal.00465.2016
[Indexed for MEDLINE]
Free PMC Article

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