Muscle reflex in heart failure : role for angiotensin II and oxidative stress
Project/Area Number |
22790226
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
|
Research Institution | Tottori University |
Principal Investigator |
KOBA Satoshi 鳥取大学, 医学部, 講師 (40565743)
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
Keywords | 活性酸素 / 運動 / 循環器疾患 / 心不全 / 活動筋反射 / 中枢コマンド / 高血圧 / 交感神経 / 自律神経機能不全 |
Research Abstract |
The present study was conducted to test the hypothesis that increased renin-angiotensin system activity in cardiovascular disease including heart failure induces oxidative stress in skeletal muscle, thereby exaggerating the muscle reflex. Rats were implanted with an osmotic-pump containing angiotensin II(AngII) for14days. In the AngII-treated rats, the muscle reflex responses(renal sympathetic nerve activity and pressor responses to hindlimb skeletal muscle contraction) were significantly larger than those in the sham-control rats. Tempol, a superoxide dismutase mimetic, reduced the muscle reflex responses in the AngII rats, but not in the sham rats. In skeletal muscle of the AngII rats, increased superoxide and upregulated gp91phox, a NADPH oxidase subunit, were observed. These results in total support our hypothesis.
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Report
(3 results)
Research Products
(14 results)