MACROPHAGE AND MYOFIBROBLAST PROLIFERATION IN REMNANT KIDNEY - ROLE OF ANGIOTENSIN-II

Local macrophage proliferation has been shown to be a major mechanism of macrophage accumulation in several immunologically-induced animal m odels of renal diseases. This study has explored whether local prolife ration of macrophages and myofibroblasts contribute to their accumulat ion in rat remnant kidney model and investigated the role of angiotens in II (Ang II) in these cellular pathological events by blocking the a ngiotensin 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 attenu ation of renal injury. In conclusion, inhibition of local macrophage a nd myofibroblast proliferation may be an important mechanism by which Ang II blockade attenuated renal injury following renal ablation.