2005 Fiscal Year Final Research Report Summary
Genetic Possibility of neuronal nitric oxide synthase for kidney disease
| Project/Area Number |
16590807
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
SERINO Ryota University of Occupational and Environmental Health, School of Medicine, Research Associate, 医学部, 助手 (00309957)
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| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Masato University of Occupational and Environmental Health, School of Medicine, Associate Professor, 医学部, 助教授 (70309962)
TAMURA Masahito University of Occupational and Environmental Health, University Hospital Kidney Center, Associate Professor, 大学病院, 助教授 (40330980)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Nitric oxide synthase / Renal failur / Glomerulosclerosis |
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| Research Abstract |
We reported the development of mice in which all three NOS isoforms are completely disrupted. Glomerulosclerosis and glomerular thrombus formation were noted in the triply n/i/eNOS^<-/-> mice but not in the wild-type mice. Quantitative analysis revealed that abnormalities, including renal tubular apotosis and glomerulosclerosis, were exacerbated in accordance with the number of disrupted NOS genes. These results suggest the NOS system plays an important role in the progression of glomerular diseases. We investigated body water balance. Urinary volume, water intake, and plasma osmolality were all significantly increased in accordance with the number of disrupted NOS genes. The triply n/i/eNOS^<-/-> mice reduced antidiuretic response to exogenous vasopressin, accompanied by impaired renal camp production. Therefore, the NOS system plays a role in maintaining homeostasis, especially in the kidney.
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