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pubmed-article:18541744pubmed:abstractTextDefects in cardiomyocyte Ca(2+) cycling are a signature feature of heart failure (HF) that occurs in response to sustained hemodynamic overload, and they largely account for contractile dysfunction. Neuronal nitric oxide synthase (NOS1) influences myocyte excitation-contraction coupling through modulation of Ca(2+) cycling, but the potential relevance of this in HF is unknown.lld:pubmed
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pubmed-article:18541744pubmed:articleTitleCardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling.lld:pubmed
pubmed-article:18541744pubmed:affiliationInstitut National de Santé et de Recherché Médicale (INSERM), Unit 689, Centre de Recherché Cardiovasculaire Lariboisière, Paris, France.lld:pubmed
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