Thimerosal, an inhibitor of endothelial acyl-coenzyme A: lysolecithin acyltransferase, stimulates the production of a nonprostanoid endothelium-derived vascular relaxing factor.

Thimerosal stimulates the production of a labile, smooth-muscle-relaxing substance in native and cultured endothelial cells. This substance is not prostacyclin (or any other prostaglandin) but has properties similar to the EDRF released by ACh or bradykinin. The production of EDRF in response to thimerosal is slower in onset, and may involve biochemical mechanisms different from those stimulated by other endothelium-dependent relaxants. The above results suggest that inhibition of acyl-CoA:lysophosphatide acyltransferase (by interaction with thiol groups of the enzyme) is the mechanism underlying the thimerosal-induced EDRF production.