Vasomotor effects of hydrogen sulfide in human umbilical vessels.

Hydrogen sulfide (HS) has recently emerged as a biologically active gas with multiple effects on the cardiovascular system. We aimed to investigate the vasomotor actions of sodium sulfide (NaS), which forms HS and HS in solution, in human umbilical artery (HUA) and vein (HUV) rings. In addition, we examined by immunocytochemistry the expression and localization of cystathionine β-synthase (CBS), cystathionine lyase (CSE), and 3-mercaptopyruvate sulphurtransferase (MPST), the enzymes responsible for endogenous HS production. Human umbilical vessels were compared with chicken embryo umbilical vessels. HUA and HUV expressed a robust signal for CSE, CBS, and 3-MPST in both endothelial and smooth muscle cells. However, HUA rings did not respond to NaS (10-10) either at resting tone or during contraction evoked by serotonin or KCl. Similarly, the extraembryonic part of chicken allantoic artery did not respond to NaS. In contrast, NaS induced a concentration-dependent contraction in HUV rings under resting tone and a concentration-dependent relaxation when the HUV rings were contracted with serotonin (42 ± 5% relaxation) or KCl (12 ± 5% relaxation). NaS-induced contraction of HUV was impaired following removal of extracellular Ca, endothelial denudation, NO synthase inhibition (L-NAME), or soluble guanylate cyclase (sGC) inhibition (ODQ). NaS-induced relaxation of HUV was impaired by the K channel inhibitor glibenclamide. In conclusion, HS does not have vasomotor effects on HUA but induced contraction (mediated through inactivation of the NO/sGC axis) and relaxation (mediated through K channels) in HUV. Our data suggest a role for HS in the venous side of human umbilical circulation.