It depends on what you mean by endothelial dysfunction. In our work in the newborn we are showing a significant link between microvascular flow and hydrogen sulfide. In addition H2S interacts with and is interacted by the other gasotransmitters, CO and NO at both genomic and enzyme levels. Whilst this can have adverse consequences ( see stark et al) it is probably more function than dysfunction. Several publications are on the way...watch this space.

There is an interesting beneficial relationship between eating garlic and CVS disease prevention which are broadly mediated by garlic compounds induced release of H2S. Read more here:

(Eating garlic is one of the best ways to lower high blood pressure and protect yourself from cardiovascular disease. A new study shows this protective effect is closely linked to how much hydrogen sulfide is produced from garlic compounds interacting with red blood cells. The researchers found this interaction triggered red blood cells to release H2S, which then led to the relaxation of blood vessels.)

Further reading: http://www.sciencedaily.com/releases/2007/10/071016131534.htm

Loss of eNOS activity is an established contributor to endothelial dysfunction. There is a dynamic competition between superoxide and lipid radicals for reaction with NO. NO only stimulates superoxide-dependent lipid oxidation when the production rate of NO is less than superoxide. H2S application augments NO bioavailability and signaling. A recent study showed that in eNOS phosphomutant mice H2S failed to rescue H2S-mediated cytoprotection.

Endothelial dysfunction is a hallmark also of preeclampsia. Recently, it was shown that plasma H2S in preeclamptic women is reduced and in a pregnant mouse model loss of H2S leads to preeclampsia like condition.

Thus the relationship between endothelial dysfunction and hydrogen sulfide exists and is also interdependent of eNOS.

http://www.ncbi.nlm.nih.gov/pubmed/24516168

Article Dysregulation of Hydrogen Sulfide (H2S) Producing Enzyme Cys...