Nitric oxide: Orchestrator of endothelium-dependent responses

Abstract

The present review first summarizes the complex chain of events, in endothelial and vascular smooth muscle cells, that leads to endothelium-dependent relaxations (vasodilatations) due to the generation of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) and how therapeutic interventions may improve the bioavailability of NO and thus prevent/cure endothelial dysfunction. Then, the role of other endothelium-derived mediators (endothelium-derived hyperpolarizing (EDHF) and contracting (EDCF) factors, endothelin-1) and signals (myoendothelial coupling) is summarized also, with special emphasis on their interaction(s) with the NO pathway, which make the latter not only a major mediator but also a key regulator of endothelium-dependent responses.

Key words::

• Atherosclerosis
• cyclo-oxygenase
• cytochrome P450 mono-oxygenase
• diabetes
• endothelin
• hypertension
• lipoxygenase
• nitric oxide synthase
• oxidative stress
• potassium channels
• soluble epoxide hydrolase
• tetrahydrobiopterin

Declaration of interest: The authors state no conflict of interest and have received no payment in preparation of this manuscript.