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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Am+Soc+Nephrol
2017 ; 28
(5
): 1350-1361
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Immunologic Effects of the Renin-Angiotensin System
#MMPMID28151411
Crowley SD
; Rudemiller NP
J Am Soc Nephrol
2017[May]; 28
(5
): 1350-1361
PMID28151411
show ga
Inappropriate activation of the renin-angiotensin system (RAS) exacerbates renal
and vascular injury. Accordingly, treatment with global RAS antagonists
attenuates cardiovascular risk and slows the progression of proteinuric kidney
disease. By reducing BP, RAS inhibitors limit secondary immune activation
responding to hemodynamic injury in the target organ. However, RAS activation in
hematopoietic cells has immunologic effects that diverge from those of RAS
stimulation in the kidney and vasculature. In preclinical studies, activating
type 1 angiotensin (AT(1)) receptors in T lymphocytes and myeloid cells blunts
the polarization of these cells toward proinflammatory phenotypes, protecting the
kidney from hypertensive injury and fibrosis. These endogenous functions of
immune AT(1) receptors temper the pathogenic actions of renal and vascular AT(1)
receptors during hypertension. By counteracting the effects of AT(1) receptor
stimulation in the target organ, exogenous administration of AT(2) receptor
agonists or angiotensin 1-7 analogs may similarly limit inflammatory injury to
the heart and kidney. Moreover, although angiotensin II is the classic effector
molecule of the RAS, several RAS enzymes affect immune homeostasis independently
of canonic angiotensin II generation. Thus, as reviewed here, multiple components
of the RAS signaling cascade influence inflammatory cell phenotype and function
with unpredictable and context-specific effects on innate and adaptive immunity.