Defecto en la homeostasis del oxido nítrico. Mecanismo común subyacente de la insulino-resistencia, la hiperactividad simpática y la morbi-mortalidad cardiovascular [Defective nitric oxide homeostasis. Common underlying mechanism between insulin resistance, sympathetic overactivity and cardiovascular morbidity and mortality]

Détails

ID Serval
serval:BIB_8A311F92E974
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Defecto en la homeostasis del oxido nítrico. Mecanismo común subyacente de la insulino-resistencia, la hiperactividad simpática y la morbi-mortalidad cardiovascular [Defective nitric oxide homeostasis. Common underlying mechanism between insulin resistance, sympathetic overactivity and cardiovascular morbidity and mortality]
Périodique
Medicina
Auteur(s)
Schwab M., Bloch J., Duplain H., Sartori C., Scherrer U.
ISSN
0025-7680
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
68
Numéro
3
Pages
243-50
Langue
espagnol
Notes
Publication types: English Abstract ; Journal Article ; Review
Résumé
Obesity, insulin resistance and associated cardiovascular complications are reaching epidemic proportions worldwide and represent a major public health problem. Over the past decade, evidence has accumulated indicating that insulin administration, in addition to its metabolic effects, also has important cardiovascular actions. The sympathetic nervous system and the L-arginine-nitric oxide pathway are the central players in the mediation of insulin's cardiovascular actions. Based on recent animal and human research, we demonstrate that both defective and augmented NO synthesis represent a central defect triggering many of the metabolic, vascular and sympathetic abnormalities characteristic of insulin-resistant states. These observations provide the rationale for the use of pharmaceutical drugs releasing small and physiological amounts of NO and/or inhibitors of NO overproduction as a future treatment for insulin resistance and associated comorbidities.
Mots-clé
Animals, Biological Availability, Cardiovascular Diseases/etiology, Cardiovascular Diseases/physiopathology, Endothelium, Vascular/drug effects, Endothelium, Vascular/metabolism, Homeostasis, Humans, Hypertension/etiology, Hypertension/physiopathology, Hypoglycemic Agents/pharmacology, Insulin/pharmacology, Insulin Resistance/physiology, Nitric Oxide/biosynthesis, Nitric Oxide/deficiency, Nitric Oxide Donors/pharmacology, Nitric Oxide Synthase Type I/metabolism, Nitric Oxide Synthase Type II/metabolism, Nitric Oxide Synthase Type III/metabolism, Rats, Sympathetic Nervous System/drug effects, Sympathetic Nervous System/physiopathology
Pubmed
Web of science
Création de la notice
02/10/2009 18:39
Dernière modification de la notice
20/08/2019 15:49
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