| Project/Area Number |
05404041
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Tokyo |
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Principal Investigator |
KUROKAWA Kiyoshi Univ.of Tokyo, Faculty of Medicine, Professor, 医学部(病), 教授 (30167390)
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| Co-Investigator(Kenkyū-buntansha) |
SEKI George Unive.of Tokyo, Faculty of Medicine, Clinical Associate, 医学部(病), 助手 (30206619)
TANIGUCHI Sjigeo Unive.of Tokyo, Faculty of Medicine, Clinical Associate, 医学部(病), 助手 (50188380)
NAKAO Akihide Unive.of Tokyo, Faculty of Medicine, Clinical Associate, 医学部(病), 助手 (10159056)
NOSAKA Kazuo Unive.of Tokyo, Faculty of Medicine, Clinical Associate, 医学部(病), 助手 (70150274)
WATANABE Tsuyoshi Univ.of Tokyo, Faculty of Medicine, Associate Professor, 医学部(病), 助教授 (80158641)
高市 憲明 東京大学, 医学部(分), 助手 (00175423)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥38,000,000 (Direct Cost: ¥38,000,000)
Fiscal Year 1995: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 1994: ¥10,800,000 (Direct Cost: ¥10,800,000)
Fiscal Year 1993: ¥23,000,000 (Direct Cost: ¥23,000,000)
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| Keywords | mesangial cells / hypertension / insulin like growth factor-I (IGF-I) / chloride / Ca signal / tubular function / prostaglandin / 糸球体機能 / クロライド / インスリン様成長因子(IGF-I) / 尿細管糸状体フィードバック / 副甲状腺関連ペプチド(PTHrP) / ネフロン / 糸球体メサンギウム細胞 / クロライドチャネル / Na-H輸送体 / アンチセンス / RT-PCR / TGF / 微量循環法 / 副甲状腺ホルモン関連ペプチド(PTHrP) / Na / H-antiporter / β-レセプター / エンドセリン / 近位尿細管 |
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| Research Abstract |
The findings of the present research project include ; 1) in contrast to mesangial cells from normotensive rat, enhanced prostaglandin production and attenuation of Ca signal and contraction when extracellular Cl concentration was decreased were absent in mesangial cells of spontaneously hypertensive rat (SHR) and Dahl salt sensitive hypertensive rat (DS) ; 2) normal mesangial cell Ca signal and contraction was attenuated by insulin like growth factor (IGF)-I receptor activation ; 3) modulation of mesangial cell Ca signal and contraction by IGF-I was absent in SHR mesangial cells but present in DS mesangial cells ; 4) IGF-I infusion had no effect on GFR in SHR while it increased GFR in normotensive control rat ; 5) Na/H exchanger-I was present only on the basolateral side of LLCPK-1 cells ; 6) analysis of beta1 receptor mRNA expression revealed its expression in distal tubule ; and 7) Cl conductance was present on the basolateral side of rabbit proximal tubule.
Furthermore, we advanced our hypothesis that disturbance of mesangial cell regulation in this research project underlies the development of hypertension via altered glomerular hemodynamics including disturbed tubuloglomerular feedback.
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