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Review
. 2016 Aug;68(2):289-96.
doi: 10.1161/HYPERTENSIONAHA.116.06591. Epub 2016 Jun 27.

Interactions Between the Immune and the Renin-Angiotensin Systems in Hypertension

Nathan P Rudemiller  1 , Steven D Crowley  2
Affiliations
Review

Interactions Between the Immune and the Renin-Angiotensin Systems in Hypertension

Nathan P Rudemiller et al. Hypertension. 2016 Aug.
No abstract available

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Figures

Figure 1
Figure 1
Interactions between the renin angiotensin system (RAS) and immune system during the pathogenesis of hypertension. Inappropriate RAS activation increases circulating Ang II. Elevated Ang II directly promotes sodium retention in the kidney and systemic vascular constriction. During hypertension, T cells and monocytes/macrophages accumulate in the kidney and vasculature where they mediate tissue injury and deleterious remodeling. Immune cells harbor the type 1 Ang II receptor, AT1A. In an apparent feedback mechanism, ligation of the AT1A receptor constrains T cell accumulation around the renal blood vessels, and activation of the AT1A receptor on T cells and macrophages limits their differentiation toward the pro-inflammatory Th1 and M1 subsets, respectively. This inhibition of Th1 and M1 polarization attenuates damage to the kidney during hypertension and mitigates the emergence of renal fibrosis that culminates in organ failure.
See this image and copyright information in PMC

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