Project/Area Number |
09670710
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Nagoya University |
Principal Investigator |
KAMIYA Kaichiro Nagoya Univ.Res.Inst.of Environ.Med., Associate Professor, 環境医学研究所, 助教授 (50194973)
|
Co-Investigator(Kenkyū-buntansha) |
KANBE Fukushi Nagoya Univ.Res.Inst.of Environ.Med., Associate Professor, 環境医学研究所, 助教授 (00211871)
YASUI Kenji Nagoya Univ.Res.Inst.of Environ.Med., Associate Professor, 環境医学研究所, 助手 (70283471)
外山 淳治 名古屋大学, 環境医学研究所, 教授 (20023658)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
|
Keywords | thyroid hormone / action potential / potassium channels / gene / cardiac hypertrophy / ion channels / アミオダロン |
Research Abstract |
In this study. we examined the modulation of cardiac potassium channels in various types of pathological conditions and during developmental changes. Possible role of gene regulation of channels was also examined. Levels of K channel mRNA.levels of channel protein, spatial distribution channel protein and ion currents were observed in cultured cardiac myocytes or hypertrophied hearts. Main findings obtained during this grant were : 1) Thyroid hormone exhibit diffeerent effects on each cardiac channels. 2) The prolongation of action potential duration in monocrotalin-induced right ventricular hypertrophy was caused initially by increase in calcium current and lately by decrease in transient outward current. 3) Effects on cardiac channels were dependent on the types of cardiac hypertrophy. differently modulated depends. All of above findings have already accepted to publish in journals listed later. The molecular methods used in this study were all developed in these ten years. These remarkable progresses in methodology may lead to further understanding of channel behavior in diseased hearts.
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