| Project/Area Number |
10670635
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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 | Niigata University |
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Principal Investigator |
AIZAWA Yoshifusa Departmen of Medicine, Niigata Univ., Professor, 医学部, 教授 (50143780)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Tadashi Kidney Research Institute, Niigata Univ. Professor, 医学部, 教授 (30092737)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Ionic channel / Antiarrhymic drugs / Thyroid hormone / Electrophysiology / 心筋 / カリウムチャネル |
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| Research Abstract |
A limitation of antiarrhytmic drug therapy is now well known and many antiarrhythmic drugs have been shown to worsen the prognosis of patients with, arrhythmias. This may be partly due to the fact that we have only limited knowledge about the modulation of gene expression of ionic channels by antiarrhythmic drugs.
When we administered amiodarone, and changes in voltage-gated K-channels were observed as quantitated by mRNAs. T3 or experimental hypothyroid state was shown clearly affect the gene-expression of K-channels. Since amioradone modifies the thyroid function, this drug will affect ionic-channels of heart directly or indirectly. Furthermore, when class I drugs which reduce the Na-currents through Na-channel were given, they affect the gene expression of Na-channel or Ca-channel. Intracelluar ca concentration seems to play a key role in regulation of the ionic channels in the heart and it is now under examination. An injury to cardiomyocytes was found to induce the un-differenation of cardiac cells resulting in gene-expression of some receptor which was exclusively observed in fetus.
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