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. © 2012 Informa UK, Ltd.
CITATION STYLE
Félétou, M., Köhler, R., & Vanhoutte, P. M. (2012, November). Nitric oxide: Orchestrator of endothelium-dependent responses. Annals of Medicine. https://doi.org/10.3109/07853890.2011.585658
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