2014 Fiscal Year Final Research Report
Mechanism of spironolactone-induced Ca2+ increase in rat testicular arteriole smooth muscle cells revealed by real-time laser confocal scanning microscopy.
| Project/Area Number |
24590259
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Iwate Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUURA Makoto 岩手医科大学, 薬学部, 講師 (00405846)
SATOH Yoh-ichi 岩手医科大学, 医学部, 教授 (40118253)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 細動脈 / spironolactone / Gタンパク / 細胞内カルシウムイオン / 共焦点レーザー顕微鏡 |
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| Outline of Final Research Achievements |
We reported that spironolactone(SP) induced an increase in intracellular Ca2+ concentration ([Ca2+]i) in rat testicular arterioles. In this study, we further investigated the mechanism of SP-induced [Ca2+]i dynamics. The increase in [Ca2+]i induced by SP was inhibited in extracellular Ca2+-free conditions. In contrast, U73122 did not affect this [Ca2+]i increase in similar to what was observed for 2-APB. H89 partially inhibited this increase, whereas GF109203X did not. Either suramin or NF449, partially blocked these [Ca2+]i increases. Similarily, either mifepristone or flutamide partially blocked the SP-induced increase in [Ca2+]i. We suggest that SP-induced increase in [Ca2+]i is mediated both by Ca2+ influx from outside and by Ca2+ mobilization from Ca2+ stores, with the former being dominant. We propose that SP interacts with both extracellular and intracellular receptors in testicular arterioles, which is followed by [Ca2+]i increases that causes smooth-muscle contraction.
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| Free Research Field |
細胞生物学
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