Hydrogen sulfide (H2S) is a unique gasotransmitter that shares many common targets with NO and CO but acts via different molecular mechanisms [1]. In the blood vessels, H2S is mostly generated in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), catalyzed by cystathioinine gamma-layse (CSE). EC-generated H2S stimulates the opening of IKCa/SKCa channels and causes VSMC hyperpolarization, fulfilling the role of endothelium-derived hyperpolarizing factor (EDHF) [2,3,4]. VSMC-generated H2S stimulates KATP channels and also causes VSMC hyperpolarization [5]. Consequently, voltage-dependent calcium channels in VSMCs are inactivated and intracellular free calcium level drops. The interaction of H2S with IKCa/SKCa as well as KATP channels is accomplished via post-translational modification of selective cysteine residues of respective ion channel proteins [6]. Whether H2S directly acts on voltage-dependent calcium channels in VSMCs is uncertain and future study in this direction is warranted. By modulating intracellular free calcium levels, H2S actively participates in the regulation of numerous cellular events, including migration, growth, proliferation, senescence, apoptosis, contraction and secretion.