| Project/Area Number |
22590236
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
IRUKAYAMA Yoko 筑波大学, 分子行動科学研究コア, 研究員 (90312834)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKOSHI Nobuyuki 筑波大学, 医学医療系, 講師 (80447218)
SAKURAI Takeshi 金沢大学, 医学系, 教授 (60251055)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 生理活性 / ストレス / 循環器 / 高血圧 / 循環器・高血圧 |
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| Research Abstract |
In this study, we analyzed of the neuropeptide W (NPW) its receptor(NPBWR1), in autonomic functional regulation under stress, using NPB/WR1 deficient (Npbwr-/-) mice. The urinary catecholamines amount of Npbwr-/- mice was increased. To elucidate the role of NPW-NPBWR1 on acute stress, we created a stress model after having contact with the intruder, C57/BL6J mice for 30 minutes. We monitored heart rate, activity, and body temperature using a telemetry system. In Npbwr1-/- mice, recovery to the steady state of the heart rate after contact with the intruder was very slow compared with wild type mice. In Npbwr-/- mice, cardiac hypertrophy was increased in comparison with wild-type mice. After administration of angiotensin II to Npbwr-/- mice, the cardiac hypertrophy deteriorated significantly as compared with wild-type mice.
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