| Project/Area Number |
01570356
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SASAKI Sei Tokyo Medical and Dental University, Assistant Professor, 医学部, 講師 (60170677)
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| Co-Investigator(Kenkyū-buntansha) |
KUWAHARA Michio same as above Instructor, 医学部, 助手
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1990: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Nephron segments / Urinary acidification / PTH / Aldosterone / Na / H exchange / Cl / HCO_3 / Na-HCO_3 cotransport / Acidosis / 水・電解質 / 電解質輸送 / ホルモン / 酸塩基平衡 |
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| Research Abstract |
1. Proximal Nephron. PTH effects on H/HCO_3 transport in rabbit proximal convoluted tubules were examined. PTH inhibited luminal Na/H exchange by 40%, whereas it did not effect basolateral Na-HCO_3 contransport. This effect was mimicked by CAMP, but not by PKC activation. Thus, PTH inhibits proximal acidification by selectively atlenuatiny luminal Na/H exchange through CAMP dependent signalling systems.
2. Distal Nephron. Two cell types were : devtified by functional and morphological respects in rabbit outer medullary collecting duct. Principal Cells (PC) had basolateral Na/H exchange and Na-HCO_3 cotransport, but no luminal H/HCO_3 transporter. Intercalated Cells (IC) had a luminal H pump and basolateral Cl/HCO_3 exchange. Chronic DOCA treatment, but not chronic acidosis stimulated both luminal H pump and basolateral Cl/HCO_3 exchange activities of IC. Thus, IC participate in urinary acidification, and its function is regulated by aldosterone.
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