| Project/Area Number |
02670453
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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 |
Pediatrics
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| Research Institution | Fukushima Medical College |
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Principal Investigator |
SUZUKI Junzo Fukushima Medical College, Pediatrics, Research Associate, 医学部小児科学講座, 講師 (20171217)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Hitoshi Fukushima Medical College, Pediatrics, Professor, 医学部小児科学講座, 教授 (80045682)
弓削田 英知 福島県立医科大学, 医学部・小児科学, 講師 (90136995)
加藤 一夫 福島県立医科大学, 医学部・小児科学, 助教授 (40136990)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1992: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Signal transduction / TXA_2 receptor / PGE_2 receptor / Phosphatidylinositol / Nephrotic syndrome / Aminonucleoside nephrotic rat / Corticosteroid / Sairei-to / PGE_2受容体 / Phospatidylinositol / thromboxane A_2(TxA_2)受容体 / 腎糸球体TxA_2産生 / ネフロ-ゼラット / ネフロ-ゼ症候群 / Phosphatidylinositol / adenylate cyclase / アミノヌクレオシド ネフロ-ゼラット |
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| Research Abstract |
Prostaglandin(PG)E_2- and thromboxane(TX)A_2- induced signal transduction were investigated in preparations derived from normal and puromycin aminonucleoside (AN) nephrotic rat (NR) kidneys.
The obtained results were as follows :
1) TXA_2 & PGE_2 production in the glomeruli of the ANNR were significantly greater than that in the glomeruli of the control rat.
2) PGE_2 receptors of the normal rat kidney were distributed in the medulla more than in the cortex, but TXA_2 receptors were in the cortex more than in the medulla.
3) The affinities of PGE_2 and TXA_2 receptors in ANNR kidneys were lower than those in normal rat kidneys.
4) Phosphatidylinositol(PI) breakdown was elicited by PGE_2 dose-dependently, and PGE_2-induced PI breakdown was significantly suppressed in ANNR kidneys.
5) The affected responsiveness of the PI breakdown system to PGE_2 in ANNR kidneys was presumed to be normalized by corticosteroid and/or Sairei-to.
These results indicate that the signal transduction of PGE_2 and/or TXA_2 receptors may be damaged in ANNR kidneys. Therefore, PGE_2 and/or TXA_2 receptors were considered to play an important role in a pathophysiology of the signal transduction in the nephrotic syndrome.
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