| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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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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