Ranolazine Attenuates the Enhanced Reverse Na⁺-Ca²⁺ Exchange Current via Inhibiting Hypoxia-Increased Late Sodium Current in Ventricular Myocytes
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- Wang Xiao-Jing
- Cardio-Electrophysiological Research Laboratory, Medical College, Wuhan University of Science and Technology, China
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- Wang Lei-Lei
- Cardio-Electrophysiological Research Laboratory, Medical College, Wuhan University of Science and Technology, China
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- Fu Chen
- Cardio-Electrophysiological Research Laboratory, Medical College, Wuhan University of Science and Technology, China
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- Zhang Pei-Hua
- Cardio-Electrophysiological Research Laboratory, Medical College, Wuhan University of Science and Technology, China
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- Wu Ying
- Cardio-Electrophysiological Research Laboratory, Medical College, Wuhan University of Science and Technology, China
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- Ma Ji-Hua
- Cardio-Electrophysiological Research Laboratory, Medical College, Wuhan University of Science and Technology, China
書誌事項
- タイトル別名
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- Ranolazine Attenuates the Enhanced Reverse Na<sup>+</sup>-Ca<sup>2+</sup> Exchange Current via Inhibiting Hypoxia-Increased Late Sodium Current in Ventricular Myocytes
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抄録
Ranolazine (RAN), a novel antianginal agent, inhibits the increased late sodium current (INa.L) under many pathological conditions. In this study, the whole-cell patch-clamp technique was used to explore the effects of RAN on INa.L and reverse Na+/Ca2+ exchange current (INCX) in rabbit ventricular myocytes during hypoxia.Tetrodotoxin (TTX) at 2 μM or RAN at 9 μM decreased significantly INa.L and reverse INCX under normoxia and RAN had no further effects on both currents in the presence of TTX. RAN (3, 6, and 9 μM) attenuated hypoxia-increased INa.L and reverse INCX in a concentration-dependent manner. Hypoxia-increased INa.L and reverse INCX were inhibited by 2 μM TTX, whereas 9 μM RAN applied sequentially did not further decrease both currents. In another group, after both currents were decreased by 9 μM RAN, 2 μM TTX had no further effects in the presence of Ran. In monophasic action potential (MAP) recording, early after-depolarizations (EADs) were suppressed by RAN (9 μM) during hypoxia. In conclusion, RAN decreased reverse INCX by inhibiting INa.L in normoxia, concentration-dependently attenuated the increase of INa.L, which thereby decreased the reverse INCX, and obviously relieved EADs during hypoxia.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 124 (3), 365-373, 2014
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205180872448
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- NII論文ID
- 130003391493
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC2cXlsF2ms7g%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 025362579
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- PubMed
- 24572816
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可