Hana Itani
Last active: 4/26/2016

Memories that last in hypertension.

Itani HA, Harrison DG
Am J Physiol Renal Physiol. 2015 308 (11): F1197-9

PMID: 25834073 · PMCID: PMC4451327 · DOI:10.1152/ajprenal.00633.2014

In recent years, it has become clear that the immune system contributes to the genesis of hypertension. Hypertensive stimuli, such as angiotensin II, DOCA-salt, and norepinephrine, cause T cells and monocytes/macrophages to accumulate in the kidney and vasculature. These cells release inflammatory cytokines, such as IL-6, interferon-γ, and IL-17, that promote renal and vascular dysfunction. These cytokines also promote angiotensinogen production in the proximal tubule and Na(+) retention in the distal nephron and contribute to renal fibrosis and glomerular damage. For several years, we have observed accumulation of memory T cells in the kidney and vasculature. Given the propensity for memory cells to produce cytokines such as interferon-γ and IL-17, interventions to prevent the formation or renal accumulation of specific memory T cell subsets could prevent end-organ damage and blood pressure elevation in response to hypertensive stimuli.

Copyright © 2015 the American Physiological Society.

MeSH Terms (8)

Animals Blood Pressure Cytokines Humans Hypertension Kidney Kidney Diseases T-Lymphocytes

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