2005 Fiscal Year Final Research Report Summary
Ectopic activities in pulmonary veins initiating atrial fibrillation
| Project/Area Number |
16590673
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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 | Nagoya University |
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Principal Investigator |
HONJO Haruo Nagoya University, Research Institute of Environmental Medicine, Associate Professor, 環境医学研究所, 助教授 (70262912)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIYA Kaichiro Nagoya University, Research Institute of Environmental Medicine, Professor, 環境医学研究所, 教授 (50194973)
KODAMA Itsuo Nagoya University, Research Institute of Environmental Medicine, Professor, 環境医学研究所, 教授 (30124720)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Atrial fibrillation / Pulmonary vein / Ion channels / Stretch / Electrophysiology |
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| Research Abstract |
Spontaneous electrical activities originating from the pulmonary vein myocardial sleeves play important roles in the initiation and maintenance of atrial fibrillation, but little is known about the ionic mechanisms of arrhytmogenic activities in the pulmonary veins. We investigated ion channel expression in rabbit and rat pulmonary veins and compared those in the sinoatiral node and atrial muscle. Hyperpolarization-activated channels (HCN1, HCN4) and Cav1.3 L-type Ca channel mRNAs were abundantly expressed in the sinoatrial node but their expression in the pulmonary veins was less than in the atrial muscle. Inward rectifier K channels (Kir2.1, Kir2.2), cardiac type Na channel (Nav1.5) and Ca-handling proteins (ryanodine receptor and SERCA) mRNAs were lower in the pulmonary veins than in atrial muscle. These results suggest that the unique ion channel expression profile in the pulmonary veins may underlie arrhythmogenic substrates such as impaired conduction and intracellular Ca overload.
Atrial fibrillation is often associated with atrial dilatation. We investigated the effects of stretch-activated channel (SAC) blockers on the vulnerability of atrial fibrillation in intra-atrial pressure-overloaded rabbit hearts. Ga^<3+> reduced the stretch-induced vulnerability. Synthesized peptides, which are reported to block a subset of SAC, and Cl^-channel blockers have no significant effects on atrial fibrillation propensity during pressure overload. Blockade of SAC might be a novel antiarrhythmic approach to atrial fibrillation under conditions of increased atrial pressure.
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[Journal Article] Computer three-dimensional reconstruction of the sinoatrial node.2005
Author(s)
Dobrzynski H, Li J, Tellez J, Greener ID, Nikolski VP, Wright SE, Parson SH, Jones SA, Lancaster MK, Yamamoto M, Honjo H, Takagishi Y, Kodama I, Efimov IR, Billeter R, Boyett MR.
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Journal Title
Circulation 111
Pages: 846-854
Description
「研究成果報告書概要(欧文)」より
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