This study was performed using adult male albino rats and acute tubular necrosis was induced by glycerol injection into the hind limbs. Inhibitors for angiotensin converting enzyme (ACE), prostaglandins (PG) and nitric oxide (NO) synthase were injected intraperitonealy before and after glycerol injection to study their roles in acute renal failure and the possibility of their interaction in the kidney in a similar pattern to that takes place in the heart. Tubular damage occurring was semi-quantified in kidneys of different groups. ACE inhibitor (perindopril) was found to reduce the glycerol-induced acute tubular necrosis establishing the injurious role of angiotensin converting enzyme in the pathogenesis of this condition. Injection of either PG synthesis inhibitor (voltaren) or NO synthase inhibitor (L-NAME) has caused increase of the glycerol-induced acute tubular necrosis indicating that both prostaglandins and NO has renoprotective effects. Injection of either PG synthesis inhibitor (voltareh) or the NO synthase inhibitor (L-NAME) together with the ACE inhibitor impairs its renoprotective effect denoting that prostaglandins and NO may mediate this renoprotection.