2017 Fiscal Year Final Research Report
Angiotensin induces vasoconstriction and vasorelaxation via Rho-kinase.
| Project/Area Number |
15K07984
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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 |
Pharmacology in pharmacy
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| Research Institution | Kobe Gakuin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小野寺 章 神戸学院大学, 薬学部, 助教 (40598380)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | アンジオテンシン / ミオシン軽鎖ホスファターゼ / 血管収縮 |
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| Outline of Final Research Achievements |
Angiotensin II (Ang II), the most active component of the renin-angiotensin system, is a multifunctional hormone that plays an important role in the cardiovascular physiology and pathology. The activation of the Ang II receptor mediates vasoconstriction and proliferation of vascular smooth muscle cell. The aim of this study was to determine the mechanism underlying Ang II-induced vasoconstriction of rat aorta. Ang II-induced constriction was significantly blocked by Rho kinase inhibitor, extracellular signal-regulated kinase 1 and 2 (Erk1/2) inhibitor, epidermal growth factor receptor (EGFR) inhibitor, and Src inhibitor. Phosphorylation of myosin phosphatase target subunit 1 (MYPT1, an index of Rho kinase activity) was abrogated by inhibitors of Src, EGFR, Erk1/2, and Rho kinase. These results suggest that Ang II induced vasoconstriction in rat aorta via Src, EGFR, MEK, and Erk1/2 activation, leading to the inactivation of myosin light chain phosphatase via phosphorylation of MYPT1.
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| Free Research Field |
薬理学
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