Deficiency of Neuronal Nitric Oxide Synthase Increases Mortality and Cardiac Remodeling After Myocardial Infarction | Zendy

Roberto Magalhães Saraiva | Zendy; Khalid M. Minhas | Zendy; Shubha V.Y. Raju | Zendy; Lili A. Barouch | Zendy; Eleanor Pitz | Zendy; Karl H. Schuleri | Zendy; Koenraad Vandegaer | Zendy; Dechun Li | Zendy; Joshua M. Hare | Zendy

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Deficiency of Neuronal Nitric Oxide Synthase Increases Mortality and Cardiac Remodeling After Myocardial Infarction

Author(s) -

Roberto Magalhães Saraiva,

Khalid M. Minhas,

Shubha V.Y. Raju,

Lili A. Barouch,

Eleanor Pitz,

Karl H. Schuleri,

Koenraad Vandegaer,

Dechun Li,

Joshua M. Hare

Publication year - 2005

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.105.557892

Subject(s) - nos1 , medicine , endocrinology , nitric oxide , nitric oxide synthase , oxidative stress , contractility , xanthine oxidase , myocardial infarction , cardiology , chemistry , biochemistry , enzyme

Neuronal nitric oxide synthase (NOS1) plays key cardiac physiological roles, regulating excitation-contraction coupling and exerting an antioxidant effect that maintains tissue NO-redox equilibrium. After myocardial infarction (MI), NOS1 translocates from the sarcoplasmic reticulum to the cell membrane, where it inhibits beta-adrenergic contractility, an effect previously predicted to have adverse consequences. Counter to this idea, we tested the hypothesis that NOS1 has a protective effect after MI.

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