| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
In the model with myocardial infarction-induced heart failure, astrocytes with angiotensin II type I receptor (AT1R) and microglia were abnormally increased at vasomotor center (rostral ventrolateral medulla; RVLM), gates of hormonal inputs into brain (paraventricular nucleus; PVN) and gates of afferent neural inputs into the brain (nucleus tractus solitarius; NTS). Prior blockade of AT1R at specific astrocytes of NTS and RVLM of myocardial infarction-induced heart failure decreased sympathoexcitaion and left ventricular end-diastolic pressure (LVEDP).
Moreover, artificial controlled afferent neural input and hormonal input increased AT1R at astrocytes of NTS and PVN respectively, and finally activated RVLM via upregulation of AT1R at astrocytes worsened hemodynamics of heart failure through the increased sympathetic activity and LVEDP.
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