| Project/Area Number |
15K18883
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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 |
Pharmacology in pharmacy
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| Research Institution | National Institute for Physiological Sciences |
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Principal Investigator |
Nishimura Akiyuki 生理学研究所, 生体機能調節研究領域, 特任助教 (00457152)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Gタンパク質共役型受容体 / シグナル伝達 / 心血管リモデリング / 細胞外ヌクレオチド / G蛋白質共役型受容体 |
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| Outline of Final Research Achievements |
Cardiovascular remodeling which refers to the changes in size, structure and function of tissues, is important for homeostasis. However, excess remodeling leads irreversible dysfunction of tissues, resulting cardiovascular diseases. Here, we investigated the role of purinergic P2Y6 receptor (P2Y6R) on cardiovascular remodeling. In vascular system, angiotensin II (Ang II) functions as a physiological regulator of blood pressure, but it also play a major role in the pathological hypertension. P2Y6R forms heterodimer with Ang II type 1 receptor (AT1R). Developmentally increased P2Y6R-AT1R heterodimer promoted Ang II-induced hypertrophy of vascular smooth muscle cells and hypertension. These results suggest that increased formation of P2Y6R-AT1R heterodimer with age may increase the likelihood of hypertension.
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