Figure 3.
Cellular effects of NO and H2S and their interactions. NO reacts with the active site of soluble guanylate cyclase (sGC) and produces cyclic GMP leading to vasorelaxation. NO can affect cellular proteins by producing peroxynitrite, which in turn can interact with cysteine residues to form S-nitrosothiols (RSNO). The oxidative pathway leads to modification of proteins by S-nitrosylation of cysteine residues. H2S raises cGMP levels through inhibition of phosphodiesterase 5A (PDE5A) an enzyme that catabolizes it. H2S can also interact with the sulfhydryl group of cysteines and proteins to form persulfides (R-SSH). NO can interact with H2S to form HSNO [32] and H2Sn [45]; H2S can interact with NO2− [34] or with RSNO [268–270] to produce NO. H2S can interact with membrane ion channels and/or voltage-dependent calcium channels leading to vasorelaxation in vascular smooth muscle [26].
KATP = ATP-sensitive potassium, KCa = voltage-dependent calcium channels