title: [Endothelial dysfunction in cardial failure: potential mechanisms].
abstract: From the vascular point of view, cardiac failure is characterised by increased systemic resistances secondary to an increased concentration of a number of vasoconstrictor substances and also to decreased endothelium dependent vasodilatation. Endothelial dysfunction has been described both in man and in animal models, but its causes are not well understood. Such dysfunction could be due to a decrease in the production of nitric oxide, a decrease in its vasodilator effect due to an increased degradation or an increased vasoconstrictor tone. Recent data suggests an improvement or prevention of this endothelial dysfunction observed in cardiac failure by physical training and by chronic treatment with an angiotensin converting enzyme inhibitor. The improvement or preservation of endothelial function induced by exercise or ACE inhibitor could explain some of the benefits of these treatments in terms of tissue perfusion and haemodynamic conditions.
authors.affiliation: Laboratoire de pharmacologie (Vacomed, IFRMP 23), faculté de médecine de Rouen.
authors.forename: R
authors.initials: R
authors.lastname: Varin
authors.forename: P
authors.initials: P
authors.lastname: Mulder
authors.forename: V
authors.initials: V
authors.lastname: Richard
authors.forename: C
authors.initials: C
authors.lastname: Thuillez
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D004285:Dogs; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D014661:Vasoconstriction; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase
vernacular_title: Dysfonction endothéliale dans l'insuffisance cardiaque: mécanismes potentiels.