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

  • 一原 直昭
    Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
  • 南沢 享
    Cardiovasc. Research Institute, Yokohama City Univ. Sch. Med.
  • 橋本 達夫
    Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
  • 内野 和顕
    Dept. Med. Science Cardiorenal Med., Yokohama City Univ.
  • 深水 昭吉
    Tsukuba Advanced Research Alliance, Univ. Tsukuba
  • 石川 義弘
    Cardiovasc. Research Institute, Yokohama City Univ. Sch. Med.
  • 梅村 敏
    Dept. Med. Science Cardiorenal Med., Yokohama City Univ.

書誌事項

タイトル別名
  • 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]

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詳細情報 詳細情報について

  • CRID
    1390001205729961728
  • NII論文ID
    130005449423
  • DOI
    10.14849/psjproc.2008.0_059_3
  • データソース種別
    • JaLC
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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