Abstract
BACKGROUND: Hydrogen sulfide (H(2)S) is considered to be the third gasotransmitter after carbon monoxide (CO) and nitric oxide (NO). It plays an important role in the regulation of vascular homeostasis. Vascular remodeling have has proved to be related to the impaired H(2)S generation. AIM OF REVIEW: This study aimed to summarize and discuss current data about the function of H(2)S in vascular physiology and pathophysiology as well as the underlying mechanisms. KEY SCIENTIFIC CONCEPTS OF REVIEW: Endogenous hydrogen sulfide (H(2)S) as a third gasotransmitter is primarily generated by the enzymatic pathways and regulated by several metabolic pathways. H(2)S as a physiologic vascular regulator, inhibits proliferation, regulates its apoptosis and autophagy of vascular cells and controls the vascular tone. Accumulating evidence shows that the downregulation of H(2)S pathway is involved in the pathogenesis of a variety of vascular diseases, such as hypertension, atherosclerosis and pulmonary hypertension. Alternatively, H(2)S supplementation may greatly help to prevent the progression of the vascular diseases by regulating vascular tone, inhibiting vascular inflammation, protecting against oxidative stress and proliferation, and modulating vascular cell apoptosis, which has been verified in animal and cell experiments and even in the clinical investigation. Besides, H(2)S system and angiotensin-converting enzyme (ACE) inhibitors play a vital role in alleviating ischemic heart disease and left ventricular dysfunction. Notably, sulfhydryl-containing ACEI inhibitor zofenopril is superior to other ACE inhibitors due to its capability of H(2)S releasing, in addition to ACE inhibition. The design and application of novel H(2)S donors have significant clinical implications in the treatment of vascular-related diseases. However, further research regarding the role of H(2)S in vascular physiology and pathophysiology is required.