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Cardiovascular Research Advance Access first published online on June 4, 2008
This version [Corrected Proof] published online on June 17, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn140
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Hydrogen sulphide is an inhibitor of L-type calcium channels and mechanical contraction in rat cardiomyocytes

Ying-Gang Sun, Yin-Xiang Cao, Wen-Wei Wang, Shan-Feng Ma, Tai Yao and Yi-Chun Zhu*

Key Laboratory of Molecular Medicine, The Ministry of Education, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, 138 Yi Xue Yuan Road, Shanghai 200032, P.R. China

* Corresponding author. Tel/fax: +86 21 5423 7098; E-mail address: yczhu{at}shmu.edu.cn

Aims: Hydrogen sulphide (H2S) is an endogenously generated gaseous transmitter that has recently been suggested to regulate cardiovascular functions. To date, there is no direct evidence for a potential role of H2S in regulating calcium channels in the heart. The present study aims to examine the hypothesis that H2S is a novel inhibitor of the L-type calcium channel current (ICa,L).

Methods and results: Electrophysiological measurements were performed in cardiomyocytes isolated from Wistar-Kyoto and spontaneously hypertensive rats. Bath application of 100 µM NaHS (a H2S donor) significantly reduced the time required for the repolarization of the action potential. Inhibition of the peak ICa,L by NaHS was determined to be concentration-dependent (25, 50, 100, 200, and 400 µM). NaHS inhibited the recovery from depolarization-induced inactivation. Electric field-induced [Ca2+]i transients and contraction of single cardiomyocytes and isolated papillary muscles were reduced by NaHS treatment. In contrast, caffeine induced an increase in [Ca2+]i that was not altered by NaHS. NaHS had no effect on the KATP current or on the levels of cAMP and cGMP in the current study.

Conclusion: H2S is a novel inhibitor of L-type calcium channels in cardiomyocytes. Moreover, H2S-induced inhibition of [Ca2+]i appears to be a secondary effect owing to its initial action towards ICa,L. The inhibitory effect of H2S on ICa,L requires further investigation, particularly in the exploration of new pathways involved in cardiac calcium homeostasis and disease pathology.

KEYWORDS Calcium; Ion channels; Myocytes

Time for primary review: 28 days


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