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Am J Physiol Renal Physiol. 2016 Dec 1;311(6):F1153-F1158. doi: 10.1152/ajprenal.00273.2016. Epub 2016 Aug 24.

Targeting cytokine signaling in salt-sensitive hypertension.

Author information

1
Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina steven.d.crowley@duke.edu.
2
Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina.

Abstract

Activated immune cell populations contribute to hypertension in part through inciting damage to the kidney and by provoking inappropriate sodium reabsorption in the nephron. Inflammatory mediators called cytokines produced by T lymphocytes and macrophages act on specific sodium transporters in the kidney, augmenting their activity or expression, with consequent expansion of intravascular fluid volume and cardiac output. The overlapping functions of these cytokines, each of which may activate multiple receptors, present challenges in precisely targeting inflammatory signaling cascades in hypertension. Moreover, broad immune suppression could expose the hypertensive patient to disproportional risks of infection or malignancy. Nevertheless, the possibility that incisive immunomodulatory therapies could provide cardiovascular and renal protection through both blood pressure-dependent and -independent mechanisms justifies comprehensive investigation into the relevant signaling pathways and tissue sites in which inflammatory cytokines function to exaggerate blood pressure elevation and target organ damage in hypertension.

KEYWORDS:

cytokine signaling; hypertension; organ damage

PMID:
27558557
PMCID:
PMC5210191
DOI:
10.1152/ajprenal.00273.2016
[Indexed for MEDLINE]
Free PMC Article

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