Cardiac myocyte neuronal nitric oxide synthase. New therapeutic target in heart failure?
Arch Mal Coeur Vaiss
; 98(12): 1244-8, 2005 Dec.
Article
em En
| MEDLINE
| ID: mdl-16435605
ABSTRACT
Although nitric oxide-dependent regulation of contractile function is altered in the diseased and failing heart, several aspects of nitric oxide (NO) signalling in the myocardium remain poorly understood. Some apparently contrasting findings may have arisen from the use of non-isoform-specific inhibitors of NO synthase isoforms (NOS) as compared to the use of mouse models genetically deficient or overexpressing the NOS thought to be responsible for the increase in NO production in heart failure (mainly NOS2 and NOS3). In recent years, identification of the neuronal NOS (NOS1) isoform in cardiac myocytes and the recognition of the importance of its subcellular localisation have greatly advanced the understanding of the critical role of NOS1-derived NO in the control of myocardial contractility both in the normal and failing heart. The challenge is now to confirm these emerging findings on the critical role of NOS1-derived NO in human cardiac physiology and hopefully translate them into therapy.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Óxido Nítrico Sintase
/
Miócitos Cardíacos
/
Insuficiência Cardíaca
/
Miocárdio
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Arch Mal Coeur Vaiss
Ano de publicação:
2005
Tipo de documento:
Article