NOS3 and heart failure: Similar to NO, H2S evokes vasorelaxing effects and eNOS inhibition or endothelium removal attenuates H2S‐induced vasorelaxation in rat aortic tissue.63, 64 In addition, our recent work shows that H2S donors activate eNOS and augments NO bioavailability in CSE KO mice.39 Furthermore treatment with H2S donors or modulation of the endogenous production of H2S through the cardiac specific overexpression of CSE protects against AMI and heart failure by attenuating oxidative stress, inhibiting apoptosis, and reducing inflammation.59