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Hydrogen sulfide contributes to the reduction of oxidative stress-related injury in cardiomyocytes but the underlying mechanism is still unclear. Here we investigated the role of voltage-operated calcium channels (VOCCs) as mediators of the beneficial effect of H 2 S against oxidative stress in cultured rat cardiomyoblasts (H9c2). Intracellular calcium signals were measured by fluorimetric live cell imaging and cell viability by colorimetric assay. Treatment with H 2 S donor (NaHS 10 µM) or Nifedipine (10 µM) decreased resting intracellular calcium concentration [Ca] i, suggesting that L-type VOCCs are negatively modulated by H 2 S. In the presence of Nifedipine H 2 S was still able to lower [Ca] i, while co-incubation with Nifedipine and Ni 2+ 100 µM completely prevented H 2 S-dependent [Ca] i decrease, suggesting that both L-type and T-type VOCCs are inhibited by H 2 S. In …