Role of chemokine receptor 2 in renal damage induced by deoxycorticosterone acetate-salt hypertension.
- Author:
Miao SUN
1
;
Lin CUI
;
Wei-hong LIU
;
Yuan GAO
;
Si SHEN
;
Ming-jun ZHU
;
You-ping WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Disease Models, Animal; Hypertension; chemically induced; physiopathology; Kidney; physiopathology; Male; Mice; Mice, Inbred C57BL; Receptors, CCR2; metabolism; Sodium Chloride, Dietary; toxicity
- From: Acta Academiae Medicinae Sinicae 2013;35(1):29-35
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo determine the role of chemokine receptor 2 (CCR2) in the development of salt-sensitive hypertension-induced renal damage.
METHODSWe investigated the renal damage induced by uninephrectomy and deoxycorticosterone acetate (DOCA)-salt in mice treated with or without a selective CCR2 antagonist RS504393 for 4 weeks. Sham mice underwent uninephrectomy without receiving DOCA and saline. Systolic blood pressure, urinary excretion of albumin and 8-isoprostane, creatinine clearance, glomerulosclerosis, renal tubulointerstitial injury, and renal monocyte/macrophage infiltration were measured.
RESULTSDOCA-salt treatment led to increased systolic blood pressure, increased urinary excretion of albumin and 8-isoprostane, decreased creatinine clearance, glomerulosclerosis, renal tubulointerstitial injury, and renal monocyte/macrophage infiltration compared with the sham mice (P<0.05). All of them were prevented by CCR2 inhibition (P<0.05).
CONCLUSIONBlockade of CCR2 prevents renal damage induced by DOCA-salt treatment, suggesting that CCR2-mediated monocyte/macrophage infiltration may contribute to salt-sensitive hypertension-induced renal injury.
