¹Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada

Correspondence: Rui Wang, Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada P7B 5E1. E-mail: rwang@lakeheadu.ca

Received 20 January 2009; Revised 18 March 2009; Accepted 1 April 2009; Published online 17 June 2009.

Abstract

The first endothelium-derived relaxing factor (EDRF) ever identified is a gasotransmitter, nitric oxide (NO). Recent studies have provided several lines of evidence to support the premise that hydrogen sulfide (H₂S), another gasotransmitter, is a new EDRF. H₂S production is catalyzed in mammalian cells by cystathionine -synthase (CBS) and/or cystathionine -lyase (CSE). The expression of CSE proteins and the activity of CBS have been observed in vascular endothelial cells. A measurable amount of H₂S is produced from endothelium upon muscarinic cholinergic stimulation. The endothelium-dependent vasorelaxation induced by H₂S shares many common mechanistic traits with those of endothelium-derived hyperpolarizing factor (EDHF). Deficiency in CSE expression increases blood pressure in CSE knockout mice and significantly diminishes endothelium-dependent relaxation of resistance arteries. More extensive and mechanistic studies in the future will help to determine whether H₂S is a new EDRF or the very EDHF.