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Drug Res (Stuttg) 2013; 63(04): 185-191
DOI: 10.1055/s-0033-1334881
Original Article
© Georg Thieme Verlag KG Stuttgart · New York

Taurine-magnesium Coordination Compound Attenuates Hypoxia/Reoxygenation Induced Ion Channel Dysfunction in Rat Ventricular Myocytes

L. Zhao
1   Department of Pharmacology, Tianjin Medical University, Tianjin, China
,
J.-S. Lou
1   Department of Pharmacology, Tianjin Medical University, Tianjin, China
,
Y. Kang
1   Department of Pharmacology, Tianjin Medical University, Tianjin, China
› Author Affiliations
Further Information

Publication History

received 17 August 2012

accepted 28 January 2013

Publication Date:
13 March 2013 (online)

Also available at
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Abstract

Because of the known anti-arrhythmic effects of taurine-magnesium coordination compound (TMCC), the aim of the present study was to explore the electrophysiological effects of TMCC on hypoxia/reoxygenation (H/R)-induced arrhythmias in rat ventricular myocytes. Sodium current (I Na), the L-type calcium current (I Ca,L), and the transient outward potassium current (I to) were evaluated using whole-cell patch-clamp recordings in rat ventricular myocytes following H/R injury. The H/R group significantly decreased sodium currents, while L-type calcium currents and transient outward potassium currents was significantly increased (all p<0.01). TMCC (200 and 400 μM) prevented abnormal sodium currents induced by H/R by inhibiting steady-state inactivation. It also counteracted abnormal L-type calcium currents induced by H/R by inhibiting steady-state activation and facilitating steady-state inactivation. In addition, it mitigated abnormal transient outward potassium currents induced by H/R by inhibiting steady-state activation. TMCC prevents H/R-induced arrhythmias in rat ventricular myocytes by modifying ion channel function.

Key words

arrhythmia - ion channels - hypoxia/reoxygenation - rat - myocytes
 

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