The intracellular calcium regulation by the sodium diuretic peptide hormone in the impaired ventricular myocytes.
| Project/Area Number |
17590718
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
URUSHIDA Tsuyoshi Hamamatsu University School of Medicine, Research Associnte, 医学部, 助教授 (20334980)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Hiroshi Hamamatsu University School of Medicine, Lecturer, 医学部附属病院, 講師 (30293632)
WATANABE Yasuhide Hamamatsu University School of Medicine, Professor, 医学部, 教授 (50305380)
KATOH Hideki Hamamatsu University School of Medicine, Research Associate, 医学部, 助教授 (80314029)
HAYASHI Hideharu Hamamatsu University School ofMedicine, Professor, 医学部, 教授 (50135258)
寺田 肇 浜松医科大学, 医学部附属病院, 講師 (50252177)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | ANP / BNP / calcium / Na^+ / H^+ exchanger / Ca^2+> exchange / heart failure / cardiac myocytes |
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| Research Abstract |
As for the heart protective effects of sodium diuretic peptide hormones (ANP、BNP、CNP), the Na-induced diuretic effect, the vascular dilation effect, and the inhibition of the rennin-angiotensin-aldosterone system (RAAS) have been known. The local activation of RAAS in the failing heart leads to myocyte hypertrophy, fibrosis, production of reactive oxygen species, and positive feedback of RAAS with the final production of aldosterone. The possible regulation of local RAAS by ANP and BNP is expected to directly protect failing myocardium. The main mechanism of the protection may be the reduction of cellular Ca^<2+> overlolad, which includes (1)the reduction of the Ca^<2+> excess current by cyclic GMP, (2)the activation of the SR-Ca^<2+> pump, and (3)the interaction with Na^+/Ca^<2+> exchanger and/or Na^+/H^+ exchanger. We specially took notices of the protective effects of ANP and BNP on Na^+/Ca^<2+> exchanger and Na^+/H^+ exchanger in the failing heart or in the ischemic/reperfitsion injury. We continue to investigate the effects of sodium diuretic peptide hormones on the Ca^<2+> regulating system in cardiac myocytes with possible application of sodium diuretic peptide hormones to the therapeutic strategy in heart failure.
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Report
(3 results)
Research Products
(10 results)
