| Project/Area Number |
09671600
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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 |
Urology
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| Research Institution | Tohoku University |
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Principal Investigator |
KONDA Ryuichiro Tohoku Univ., Hospital, Lecturer, 医学部・附属病院, 講師 (10225609)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Kiyohide Tohoku Univ., School of med, Research Associate, 医学部, 助手 (00271908)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | hydronephrosis / glomerular Sclerosis / tubulointerstitial injury / renin / angiotensin II / angiotensin converting enzyme / contralateral kidney / 水腎症 / 糸球体酵素 / 尿細管間質防害 / プロスタグランディンE_2 / トロンボキサンA_2 / renin / angiotensinogen / Angiotensin / 接着分子 / angiotensin II / T cell |
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| Research Abstract |
Experimental studies were performed using the rats that were subjected to left complete ureteral obstruction (UUO), left nephrectomy (UN) or sham operation (control) to evaluate the effect of unilateral hydronephrosis to the opposite healthy mate.
Kidneys were harvested 16 week or 28 weeks after surgery. Blood were simultaneously obtained from aorta of each rat to determine plasma renin activity (PRA), ACE, aldosteron, creatinine. Although levels of PRA were lower in UUO than UN and control, renal expression of immunostained renin significantly increased in the hydronephrotic kidneys but decreased in the contralateral kidneys. On the other hand, immunostaining of angiotensinogen and ACE was stronger in the opposite mates in UUO than the hyronephrotic kidneys, the remaining kidneys in UN and the right kidneys in the control. The degree of glomerular sclerosis and interstitial fibrosis was more intense in the non-hydronephrotic kidneys in UUO than the remaining kidneys in UN and the control kidneys.
Our observations indicates that the hydronephrotic kidneys appear to progress the renal injury in the contralateral kidneys via stimulating the production of angiotensin II by a renin-independentmechanism.
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