Objective: Ang (1-7) recognised as a biologically active component of renin angiotensin system (RAS). It has been documented that peripheral activity of Ang (1-7) gets reduced during diabetic nephropathy (DN) which is one of the most common cause of end stage renal disease. Peripheral activity of RAS is regulated by brain RAS. The purpose of present study is to investigate the role of brain angiotensin (1-7) in chronic hyperglycemia induced nephropathy in wistar rats. Material and methods: Diabetes mellitus (DM) is induced by single dose of alloxan (120 mg/kg: i.p.). The biochemical parameters related to DN was estimated using commercially available kits. Results: Diabetic rat, after 8 weeks of alloxan administration shows elevated serum creatinine, blood urea nitrogen, protein in urine, kidney weight/body weight and deceased level of serum nitrite. However, intracerebroventricular treatment with Ang (1-7) (4.8 μg/day) and valsartan (100 nmol/ day) (which do not cross blood brain barrier) alone and combination of Ang (1-7) and valsartan for 2 weeks markedly attenuated these changes and increased serum nitrite in DN induced rats. Conclusion: The finding of this study suggests that brain Ang (1-7) play a vital role in controlling the peripheral activity of RAS in diabetic nephropathy which may be due to the decreased central sympathetic outflow and peripheral activity of Ang II.
Key words : Ang (1-7), Diabetic nephropathy, Alloxan, Valsartan, Brain renin angiotensin system
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