| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Outline of Final Research Achievements |
Using malignant hypertension model rats (M-SHRSP) we found that activations of endoplasmic reticulum stress (ERS) and apoptotic pathway but not autophagy are involved in the pathophysiology of hypertensive renal damage. We also found that antihypertensive therapy improve renal damage by downregulating ERS pathway, though it upregulats autophagy pathways. These findings raise a possibility that ERS and autophagy could be a new therapeutic target for hypertensive renal disease, especially malignant nephrosclerosis.
On the other hand, we could not obtain any successful results in the series of physiological study. We found neither age-related alterations in the control of glomerular hemodynamics nor in the vascular reactivity of renal arterioles. In addition, we could not establish a culture system of vascular smooth muscle cells and endothelial cells of renal arterioles to study their detail cellular mechanisms.
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