• Reduced expressions of CBS and CSE may inhibit the H2 S signaling pathway, which might be one of the mechanisms underlying androgen deficiency-induced ED in rats.1
  • A review article states H₂S promotes penile erection by acting on the ATP-sensitive potassium channels to relax the vascular smooth muscle as well as by the synergistic effect with testosterone and NO to relax the corpus cavernosum smooth muscle.2
  • Exogenous H₂S [NaHS] or L-Cys causes a concentration-dependent relaxation of strips of human corpus cavernosum and promoted penile erection in rats.3
  • Intracavernous injection of sodium hydrogen sulphide to primates resulted in significant increases in penile length and cavernous pressure. Also administration of DL-propargylglycine (inhibitor of CSE) to rats resulted in significant reduction in cavernous nerve stimulation-evoked perfusion pressure.4
  • A dual action on PKA and PKG activation, ACS6 (sildenafil citrate + NaHS) promoted erection and inhibited of oxidative stress greater than NaHS alon rabbit isolated corpus cavernosum and in hypertensive rats.5
  • Endogenous H₂S production was significantly decreased in the diabetic ED rats’ penile tissues due to downregulated expression of the CAT/3-MST and DAO/3-MST pathways and low activities of CBS and CSE.6)
  • There are functional roles for H₂S in sexual medicine related to cavernosal smooth muscle relaxation and the erectile mechanism. H₂S may function in both normal endothelial and cavernosal smooth muscle function, as well as in the pathogenesis of erectile dysfunction (ED).7