| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Outline of Final Research Achievements |
This study investigated whether hyperuricemia could induce vascular and renal dysfunction. Administration of an uricase inhibitor potassium oxonate (1500mg/kg/day) increased plasma uric acid levels in uninephrectomized rats (2.7±0.1mg/dL vs. 2.0±0.1mg/dL, p<0.05）. In the hyperuricemia group, urinary protein excretion increased (11±1.2mg/day vs. 7±0.5mg/day, p<0.05) and endothelium-dependent relaxation of the aorta was impaired compared to the vehicle group, whereas there were no significant differences in blood pressure. Cilnidipine had not effect on blood pressure, but decreased plasma uric acid and proteinuria and improved vasodilatory response. These results suggest that the increase in plasma uric acid could be a risk factor for renal and vascular injury. Cilnidipine might be beneficial against renal and vascular dysfunction which relates to hyperuricemia.
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