| Project/Area Number |
23790932
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
HORITA Shoko 東京大学, 医学部附属病院, 助教 (20534895)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 高血圧学 / 高血圧 / Na輸送 / 近位尿細管 / NBCe1 / ERK / NO |
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| Research Abstract |
AngII has biphasic effect (stimulation in low concentration and inhibition in high concentration) on mouse proximal tubule (PT) but in human AngII monophasically stimulates PT transport. To clarify this, NBCe1 activity in PT was measured in human, wild-type and cGKII-/- mice kidney. In human inhibition of NO blocked AngII effect, meanwhile NO donor stimulated NBCe1 activity via ERK. In wild-type mice the inhibition by high concentration of AngII changed to stimulation by inhibition of NO, while NO donor suppressed NBCe1. It was suggested that in human PT AngII has monophasic stimulatory effect via NO and consequent ERK activation, and regulation of blood pressure by AngII is more important.
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