Journal
CARDIOVASCULAR RESEARCH
Volume 79, Issue 4, Pages 632-641Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvn140
Keywords
calcium; ion channels; myocytes
Categories
Funding
- Ministry of Science and Technology of China [2007CB512006]
- National Natural Science Foundation of China [30470628]
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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 (I-Ca,I-L). Methods and results Electrophysiological measurements were performed in cardiomyocytes isolated from Wistar-Kyoto and spontaneously hypertensive rats. Bath application of 100 mu M NaHS (a H2S donor) significantly reduced the time required for the repolarization of the action potential. Inhibition of the peak I-Ca,I-L by NaHS was determined to be concentration-dependent (25, 50, 100, 200, and 400 mu M). 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 riot altered by NaHS. NaHS had no effect on the K-ATP 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 cardionnyocytes. Moreover, H2S-induced inhibition of [Ca2+] i appears to be a secondary effect owing to its initial action towards I-Ca,I-L. The inhibitory effect of H2S on I-Ca,I-L requires further investigation, particularly in the exploration of new pathways involved in cardiac calcium homeostasis and disease pathology.
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