Identification of the Ca2+ entry pathway during hypotonicity in the principal cells of kidney cortical collecting ducts.
| Project/Area Number |
25860167
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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 |
General physiology
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| Research Institution | Iwate Medical University |
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Principal Investigator |
KOMAGIRI YOU 岩手医科大学, 医学部, 助教 (80405753)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | チャネル / 生体膜 / 低浸透圧 / カルシウムチャネル / 細胞・組織 / 生理学 / カルシウム流入 / 調節性容積減少 / 皮質集合管 |
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| Outline of Final Research Achievements |
This study was carried out to explore the Ca2+ entry pathway during hypotonicity in the principal cells of kidney cortical collecting ducts. Using cell-attached patch recordings, it was found that a nicardipine-senstitive Ca2+ entry pathway involved in the hypotonicity-induced BK channel activation. RT-PCR analysis showed the presence of transcripts of T-type Ca2+ channel in cortical collecting ducts. Under the whole-cell voltage clamp condition, the hypotonicity-activated cation current, which was nicardipine sensitive but insensitive to Gd3+ and Ni2+, was observed. In addition, the cation current was strongly inhibited by pyr3, a selective TRPC3 channel blocker. These results suggest that nicardipine and Pyr3 sensitive cation conductance, which is activated by hypotonicity, is present in the principal cells of kidney cortical collecting ducts. Further experiments are needed to identify the molecular basis underlying this conductance.
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Report
(3 results)
Research Products
(4 results)
