title: 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.
authors: Institut Recherches Servier, Suresnes, France. michel.feletou@fr.netgrs.com
authors: Michel
authors: M
authors: Félétou
authors: Ralf
authors: R
authors: Köhler
authors: Paul M
authors: PM
authors: Vanhoutte
mesh_terms: D001685:Biological Factors / Q000378:metabolism*; D019332:Endothelin-1 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D001685:Biological Factors; D019332:Endothelin-1; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide