Objective: Ion channels have important roles in maintaining cell viability and cellular functions. The aim of this study is to determine the effects of losartan on TRPV1 and TRPM2 ion channels at experimental diabetes mellitus kidney tissues in rats.

Material and Method: We used 24 male 8-10 weeks old Wistar albino rats. Rats were divided into 4 groups. No application was made to control group. To buffer group, only phosphate-citrate buffer was injected intraperitoneally. To diabetic group 50 mg/kg streptozocin (STZ) that was dissolved in phosphate-citrate buffer was injected. In diabetes + losartan group, 50 mg/kg STZ was injected and losartan was given 10 mg/kg/day orally after development of diabetes. Finally rats were decapitated and kidney tissues were removed. With routine procedures, tissues were embedded in paraphine blockes. For TRPV1 ve TRPM2 immunreactivity ‘‘avidin-biotin-peroxidase\'\' method was applied.

Results: TRPV1 immunreactivity was at +3 diffusiveness in glomeruli at control and buffer group. In comparison with control group, TRPV1 immunreactivity was decreased at diabetic group as +1 diffusiveness. There was no alteration at TRPV1 immunreactivity between diabetic group and losartan group. TRPM2 immunreactivity was observed +1 intensity in tubules at control and buffer group. In comparison with control group, TRPM2 immunreactivity was increased at diabetic group as +3 intensity. In comparison with diabetic group, TRPM2 immunreactivity was decreased at losartan group.

Conclusion: We observed that diabetes decreases TRPV1 immunreactivity, increases TRPM2 immunreactivity at rat kidney tissue. These results suggest that TRPV1 and TRPM2 channels can parcipate to pathophysiological mechanisms of diabetic nephropathy.