Local macrophage proliferation has been shown to be a major mechanism of macrophage accumulation in several immunologically-induced animal models of renal diseases. This study has explored whether local proliferation of macrophages and myofibroblasts contribute to their accumulation in rat remnant kidney model and investigated the role of angiotensin II (Ang II) in these cellular pathological events by blocking the angiotensin II activity with ramipril, an angiotensin converting enzyme (ACE) inhibitor, or valsartan, an Ang II type I receptor antagonist. There was local proliferation of macrophages and myofibroblasts within renal parenchyma following renal ablation, contributing significantly to macrophage and myofibroblasts accumulation, renal dysfunction and fibrosis. Both treatment resulted in inhibition of local proliferation of macrophages and myofibroblasts and this was associated with attenuation of renal injury. In conclusion, inhibition of local macro- phage and myofibroblast proliferation may be an important mechanism by which Ang II blockade attenuated renal injury following renal ablation.
|Journal||Kidney International, Supplement|
|Publication status||Published - 1 Dec 1997|
- Angiotensin II renal ablation
- Macrophage proliferation