We are analyzing https://link.springer.com/article/10.1007/s00395-015-0506-5.

Title:
NOS1 induces NADPH oxidases and impairs contraction kinetics in aged murine ventricular myocytes | Basic Research in Cardiology
Description:
Nitric oxide (NO) modulates calcium transients and contraction of cardiomyocytes. However, it is largely unknown whether NO contributes also to alterations in the contractile function of cardiomyocytes during aging. Therefore, we analyzed the putative role of nitric oxide synthases and NO for the age-related alterations of cardiomyocyte contraction. We used C57BL/6 mice, nitric oxide synthase 1 (NOS1)-deficient mice (NOS1−/−) and mice with cardiomyocyte-specific NOS1-overexpression to analyze contractions, calcium transients (Indo-1 fluorescence), acto-myosin ATPase activity (malachite green assay), NADPH oxidase activity (lucigenin chemiluminescence) of isolated ventricular myocytes and cardiac gene expression (Western blots, qPCR). In C57BL/6 mice, cardiac expression of NOS1 was upregulated by aging. Since we found a negative regulation of NOS1 expression by cAMP in isolated cardiomyocytes, we suggest that reduced efficacy of β-adrenergic signaling that is evident in aged hearts promotes upregulation of NOS1. Shortening and relengthening of cardiomyocytes from aged C57BL/6 mice were decelerated, but were normalized by pharmacological inhibition of NOS1/NO. Cardiomyocytes from NOS1−/− mice displayed no age-related changes in contraction, calcium transients or acto-myosin ATPase activity. Aging increased cardiac expression of NADPH oxidase subunits NOX2 and NOX4 in C57BL/6 mice, but not in NOS1−/− mice. Similarly, cardiac expression of NOX2 and NOX4 was upregulated in a murine model with cardiomyocyte-specific overexpression of NOS1. We conclude that age-dependently upregulated NOS1, putatively via reduced efficacy of β-adrenergic signaling, induces NADPH oxidases. By increasing nitrosative and oxidative stress, both enzyme systems act synergistically to decelerate contraction of aged cardiomyocytes.
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pubmed, article, google, scholar, cas, nitric, oxide, synthase, heart, physiol, cardiac, expression, central, res, nadph, ventricular, neuronal, circ, nos, calcium, oxidase, contraction, cardiomyocytes, mice, myocytes, heymes, aging, activity, betaadrenergic, zhang, regulation, rat, myocardial, failure, cell, wang, aged, role, access, circulation, human, dois, function, murine, rueckschloss, increased, nox, diabetic, shah, rats,

Topics {✒️}

month download article/chapter nitric oxide regulates nitric oxide derived nitric oxide synthase ryanodine receptor s-nitrosylation stretch-activated cation currents article basic research cardiac excitation-contraction coupling design target-specific primers l-type ca2+ current peroxynitrite-induced cardiac depression nitric oxide synthases nitric oxide regulation insulin-dependent diabetic subjects increased beta3-adrenoceptor stimulation cross bridge-dependent activation net nitrite/nitrate production mammalian cardiovascular aging beta-adrenergic inotropic responsiveness altered beta-adrenergic response full article pdf cardiomyocyte-specific nos1-overexpression beta-adrenoceptor-g-protein nitric oxide control reduced beta-adrenergic signaling smooth muscle cells decreased beta-adrenergic sensitivity induces nadph oxidases acto-myosin atpase activity conditions privacy policy protein s-nitrosylation adenylyl cyclase system guinea pig myocytes nadph oxidase expressions privacy choices/manage cookies nitric oxide nadph oxidase activity murine ventricular myocytes age-dependently upregulated nos1 cardiomyocyte-specific overexpression impairs contraction kinetics cardiac-specific overexpression beta3-adrenergic stimulation ventricular calcium current β-adrenergic signaling sears ce adenylate cyclase regulation dose-dependent regulation bendall jk coronary artery disease

Questions {❓}

Sears CE, Ashley EA, Casadei B (2004) Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?

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         headline:NOS1 induces NADPH oxidases and impairs contraction kinetics in aged murine ventricular myocytes
         description:Nitric oxide (NO) modulates calcium transients and contraction of cardiomyocytes. However, it is largely unknown whether NO contributes also to alterations in the contractile function of cardiomyocytes during aging. Therefore, we analyzed the putative role of nitric oxide synthases and NO for the age-related alterations of cardiomyocyte contraction. We used C57BL/6 mice, nitric oxide synthase 1 (NOS1)-deficient mice (NOS1−/−) and mice with cardiomyocyte-specific NOS1-overexpression to analyze contractions, calcium transients (Indo-1 fluorescence), acto-myosin ATPase activity (malachite green assay), NADPH oxidase activity (lucigenin chemiluminescence) of isolated ventricular myocytes and cardiac gene expression (Western blots, qPCR). In C57BL/6 mice, cardiac expression of NOS1 was upregulated by aging. Since we found a negative regulation of NOS1 expression by cAMP in isolated cardiomyocytes, we suggest that reduced efficacy of β-adrenergic signaling that is evident in aged hearts promotes upregulation of NOS1. Shortening and relengthening of cardiomyocytes from aged C57BL/6 mice were decelerated, but were normalized by pharmacological inhibition of NOS1/NO. Cardiomyocytes from NOS1−/− mice displayed no age-related changes in contraction, calcium transients or acto-myosin ATPase activity. Aging increased cardiac expression of NADPH oxidase subunits NOX2 and NOX4 in C57BL/6 mice, but not in NOS1−/− mice. Similarly, cardiac expression of NOX2 and NOX4 was upregulated in a murine model with cardiomyocyte-specific overexpression of NOS1. We conclude that age-dependently upregulated NOS1, putatively via reduced efficacy of β-adrenergic signaling, induces NADPH oxidases. By increasing nitrosative and oxidative stress, both enzyme systems act synergistically to decelerate contraction of aged cardiomyocytes.
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