Possible Involvement of Endothelin-1 in Cardioprotective Effects of Benidipine

この論文にアクセスする

この論文をさがす

著者

    • IKEDA Keiichi
    • Division of Nephrology and Hypertension, Department of Internal Medicine, Jikei University School of Medicine
    • TOJO Katsuyoshi
    • Division of Endocrinology and Metabolism, Department of Internal Medicine, Jikei University School of Medicine
    • TOKUDOME Goro
    • Division of Nephrology and Hypertension, Department of Internal Medicine, Jikei University School of Medicine
    • AKASHI Toshihiko
    • Division of Endocrinology and Metabolism, Department of Internal Medicine, Jikei University School of Medicine
    • HOSOYA Tatsuo
    • Division of Nephrology and Hypertension, Department of Internal Medicine, Jikei University School of Medicine
    • HARADA Masaki
    • Department of Medicine and Clinical Science, Kyoto University, Graduate School of Medicine
    • NAKAGAWA Osamu
    • Department of Medicine and Clinical Science, Kyoto University, Graduate School of Medicine
    • NAKAO Kazuwa
    • Department of Medicine and Clinical Science, Kyoto University, Graduate School of Medicine

抄録

Benidipine hydrochloride has been developed as an antagonist for the L-type calcium channel and is used as an anti-hypertensive drug. But recent studies have reported that benidipine exerts not only anti-hypertensive actions but also anti-hypertrophic actions on cardiac muscles. Endothelin-1 (ET-1), one of the endogenous pathological humoral factors of cardiovascular diseases such as hypertension and heart failure, has a strong vasoconstrictive action and could induce hypertension and cardiac hypertrophy. So, it is a matter of great interest whether or not calcium antagonists can decrease cardiac hypertrophy induced by the pathological vasoactive substances such as ET-1. Thus, the present study was designed to elucidate the effects of benidipine on cardiac hypertrophy, and particularly on the interaction with ET-1, using neonatal rat cardiac myocytes (MCs) and cardiac non-myocytes (NMCs) culture systems. Cells were cultured with or without ET-1, benidipine, and nifedipine and the effects of calcium antagonists on cardiac hypertrophy were evaluated by incorporations of [<sup>3</sup>H]-leucine and [<sup>3</sup>H]-thymidine into MCs and/or NMCs. Benidipine significantly decreased the ET-1-induced increase of [<sup>3</sup>H]-leucine and [<sup>3</sup>H]-thymidine uptake into cardiac MCs and NMCs, whereas no significant effects of nifedipine were observed. Furthermore, benidipine (10<sup>-8</sup>M) attenuated ET-1 secretions from NMCs. In summary, benidipine at least partially decreased the cardiac hypertrophy induced by paracrine mechanisms through its attenuation of ET-1 secretions from NMCs. Benidipine could thus be a useful tool for preventing cardiac hypertrophy due to hypertension. (<i>Hypertens Res</i> 2000; 23: 491-496)

収録刊行物

  • Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension

    Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension 23(5), 491-496, 2000-09-01

    The Japanese Society of Hypertension

参考文献:  34件中 1-34件 を表示

被引用文献:  3件中 1-3件 を表示

各種コード

  • NII論文ID(NAID)
    10008740403
  • NII書誌ID(NCID)
    AA10847079
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    09169636
  • データ提供元
    CJP書誌  CJP引用  J-STAGE 
ページトップへ