| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Hypertension is a well-recognized complication of autosomal dominant polycystic kidney disease (ADPKD). Hypertension relates to progressive kidney enlargement and is significant independent risk factor for progression to end-stage renal disease. However, the definite mechanisms leading to hypertension in ADPKD are not well understood. The purpose of this study is to examine the effects of antihypertensive drugs for pkd1 conditional knockout mice, and the participation of intrarenal RAS in ADPKD. We generated the pkd1 conditional knockout mice (Pkd1 KO mice). To evaluate the effects of antihypertensive drugs, Pkd1 KO mice were treated by amlodipine or olmesartan or aliskiren, or vehicle for 12 weeks. Aliskiren treatment significantly reduced renal cystic index. Aliskiren treatment group improved tubulointerstital fibrosis. Renin, Ang II and AGT expression were increased significantly in cystic kidneys. Aliskiren prevented intrarenal RAS activation and cystic progression.
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