Apelin-APJ系はカテコラミン誘発性心肥大を防止する上で重要な役割を持つ
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- 一原 直昭
- Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
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- 南沢 享
- Cardiovasc. Research Institute, Yokohama City Univ. Sch. Med.
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- 橋本 達夫
- Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
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- 内野 和顕
- Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
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- 深水 昭吉
- Tsukuba Advanced Research Alliance, Univ. Tsukuba
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- 石川 義弘
- Cardiovasc. Research Institute, Yokohama City Univ. Sch. Med.
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- 梅村 敏
- Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
書誌事項
- タイトル別名
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- Apelin-APJ System Plays an Important Role in Preventing Catecholamine-induced Cardiac Hypertrophy
説明
Background: While apelin and its endogenous receptor APJ have been reported to play roles in pathophysiology of the cardiovascular system, the relationship of apelin-APJ system with cardiac hypertrophy is still not well understood. Recently, Kuba et al. have reported that the degree of cardiac hypertrophy induced by pressure overload in apelin-deficient and wild type (WT) mice are not significantly different (2007, Circ Res). Since we had generated APJ-deficient (APJ KO) mice, we examined whether apelin-APJ system affected the pathogenesis of catecholamine-induced cardiac hypertrophy. Materials and Methods: APJ KO mice and WT mice at 3-month old (n=11, respectively) received chronic infusion of isoproterenol (ISO, 60mg/kg/day) for 7 days. Echocardiography was performed before and after infusion. Results: In the absence of ISO infusion, the heart of APJ KO mice was not morphologifcally different from that of WT mice. Excessive β-adrenergic stimulation developed significant cardiac hypertrophy in both strains, but to a greater extent in APJ KO mice (the ratio of heart weight to tibial length: 8.1±0.7 versus 7.5±0.7 mg/mm, p<0.05). Conclusion: The present study demonstrated that apelin-APJ system played an important role in preventing catecholamine-induced cardiac hypertrophy. [J Physiol Sci. 2008;58 Suppl:S59]
収録刊行物
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- 日本生理学会大会発表要旨集
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日本生理学会大会発表要旨集 2008 (0), 059-059, 2008
一般社団法人 日本生理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205729961728
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- NII論文ID
- 130005449423
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- データソース種別
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- JaLC
- CiNii Articles
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- 抄録ライセンスフラグ
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