Hydrogen sulphide in heart and systemic circulation

Inflamm Allergy Drug Targets. 2011 Apr;10(2):103-8. doi: 10.2174/187152811794776204.


In the mammalian cardiovascular system, H(2)S joins carbon monoxide (CO) and endothelial derived relaxing factors, (EDRFs)-nitric oxide (NO), as the third gasotransmitter. In the vasculature, cystathionine-γ-lyase (CSE) is the main enzyme responsible for H(2)S biosynthesis starting from the substrate e.g. L-cysteine. There is a growing body of evidence that supports a role for H(2)S in regulating the vascular homeostasis. H(2)S (NaHS) is known to induce a concentration-dependent relaxation of large conduit arteries. Interestingly, H(2)S also relaxes peripheral resistance vessels such as mesenteric arteries suggesting a role for H(2)S also in the regulation of vascular resistance and systemic blood pressure. This vasodilatory effect is dependent on the activation of K(ATP) channels. However, a cross-talk exists between the L-Argine/NO and L-cysteine/H(2)S pathways. Furthermore, it has been shown that H(2)S acts as an endogenous non-selective inhibitor of phosphodiesterase activity. Compelling evidence links H(2)S to regulation of erectile function while it remains unclear whether the L-cysteine/H(2)S pathway plays a pathogenetic role in erectile dysfunction. Despite the rapid growth of the field, it should be noted that several aspects of H(2)S physiology in the cardiovascular system remain unsolved and the lack of reliable inhibitors and donors remains a major limitation.

Publication types

  • Review

MeSH terms

  • Animals
  • Blood Pressure / physiology
  • Cardiovascular System / metabolism*
  • Homeostasis
  • Humans
  • Hydrogen Sulfide / metabolism*
  • KATP Channels / metabolism
  • Phosphoric Diester Hydrolases / drug effects
  • Vasodilation / physiology*


  • KATP Channels
  • Phosphoric Diester Hydrolases
  • Hydrogen Sulfide