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Cardiovascular Research Advance Access [Accepted Manuscript] published online on June 4, 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 sulfide 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*

Department of Physiology and Pathophysiology and the Key Laboratory of Molecular Medicine the Ministry of Education, Fudan University Shanghai Medical College, Shanghai, China

* Correspondence author: Prof. Yi-Chun Zhu, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, 138 Yi Xue Yuan Road, Shanghai 200032, China; E-mail: yczhu{at}shmu.edu.cn; Tel: +86-21-5423 7098; Fax: +86-21-5423 7098

Aims: Hydrogen sulfide (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: Electrophysiological measurements were performed in cardiomyocytes isolated from Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR).

Results: Bath application of 100 µM NaHS (a H2S donor), significantly reduced the time required for 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 the levels of cAMP and cGMP in the current study.

Conclusions: 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 due 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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