Signaling pathways for the vascular effects of hydrogen sulfide.

PURPOSE OF REVIEW

The physiological and pathophysiological importance of endogenous hydrogen sulfide to cardiovascular health has been recognized in recent years. The signaling mechanisms underlying the multifaceted vascular effects of H2S, on the contrary, have been unclear. This article reviews recent literature on cellular and molecular events triggered or modulated by H2S in the vascular system over the period of 2009-2010.

RECENT FINDINGS

H2S causes protein S-sulfhydration. The activation of ATP-sensitive K channels (KATP channels) by H2S likely occurs as the result of specific cysteine residues of KATP channel proteins being S-sulfhydrated. Produced in endothelial cells and inducing smooth muscle hyperpolarization, H2S appears to functioning as an endothelium-derived hyperpolarizing factor. The inhibition of phosphodiesterases by endogenous H2S is an additional exciting discovery, which offers answers for the differential vascular effects of this gasotransmitter due to the tissue-specific distribution of different isozymes of phosphodiesterases. Furthermore, endothelial cells and smooth muscle cells have opposite growth responses to H2S stimulation, involving the same sets of signaling molecules.

SUMMARY

An array of signaling pathways in vascular tissues is enlisted by endogenous H2S. An insightful understanding of these signaling mechanisms would help elucidate the pathogenesis of selective cardiovascular diseases and develop related therapeutic interventions by targeting H2S metabolism.