Role of Brain Angiotensin-II in Development of Experimental Diabetic Nephropathy in Wistar Rats

The renin-angiotensin-aldosterone system (RAAS) plays a key role in diabetic nephropathy (DN). Angiotensin-II secreted during the RAAS pathway increases nephropathy. It stimulates oxidative stress which can quench nitric oxide. Reduced oxide level aggravates Ang-II-induced vasoconstriction. Ang-II has also emerged as central mediator of glomerular hemodynamic changes that are associated with renal injury. Deletion ACE2 is noted due to increased leads development DN. We hypothesize caused by periphery may be controlled brain RAAS. ACE inhibitors and ARBs show renoprotective effect when administered through ICV without crossing blood-brain barrier. DN was observed after 8 weeks diabetes induction alloxan. Administration captopril valsartan once combined therapy for 2 weeks, significantly reduced urine output, blood urea nitrogen, total protein urine, serum cholesterol, creatinine, triglycerides, kidney/body weight ratio compared control rats. Further, combination body nitrate animals. However, levels reduce sympathetic outflow might have decreased peripheral activity shows beneficial effects