We are analyzing https://link.springer.com/article/10.1007/s11010-009-0219-x.

Title:
Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart | Molecular and Cellular Biochemistry
Description:
Nitric oxide (NO) produced in the heart by nitric oxide synthase (NOS) is a highly reactive signaling molecule and an important modulator of myocardial function. NOS catalyzes the conversion of l-arginine to l-citrulline and NO but under particular circumstances reactive oxygen species (ROS) can be formed instead of NO (uncoupling). In the heart, three NOS isoforms are present: neuronal NOS (nNOS, NOS1) and endothelial NOS (eNOS, NOS3) are constitutively present enzymes in distinct subcellular locations within cardiomyocytes, whereas inducible NOS (iNOS, NOS2) is absent in the healthy heart, but its expression is induced by pro-inflammatory mediators. In the tissue, NO has two main effects: (i) NO stimulates the activity of guanylate cyclase, leading to cGMP generation and activation of protein kinase G, and (ii) NO nitrosylates tyrosine and thiol-groups of cysteine in proteins. Upon nitrosylation, proteins may change their properties. Changes in (i) NOS expression and activity, (ii) subcellular compartmentation of NOS activity, and (iii) the occurrence of uncoupling may lead to multiple NO-induced effects, some of which being particularly evident during myocardial overload as occurs during aortic constriction and myocardial infarction. Many of these NO-induced effects are considered to be cardioprotective but particularly if NOS becomes uncoupled, formation of ROS in combination with a low NO bioavailability predisposes for cardiac damage.
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Keywords {🔍}

google, scholar, nitric, oxide, synthase, heart, cardiac, myocardial, res, failure, circ, endothelial, physiol, inducible, circulation, neuronal, cell, mice, nos, hypertrophy, ventricular, function, expression, protein, infarction, role, human, article, calcium, regulation, sci, remodeling, kinase, left, biol, usa, overexpression, hypertension, ryanodine, receptor, pharmacol, myocytes, mol, cardiol, cardiovasc, proc, natl, acad, failing, van,

Topics {✒️}

g-monomethyl-l-arginine xod inducible nitric-oxide synthase month download article/chapter cardiac excitation-contraction coupling cytokine-induced nitric oxide sarcoplasmic reticulum ca2+-atpase camp-dependent protein kinase nitric oxide regulates nitric oxide derived l-type calcium channels integrin stimulation-induced hypertrophy van der laarse cyclic gmp-dependent mechanism β-adrenergic receptor therapy fas-induced caspase denitrosylation arg-gly-asp motif end-stage heart failure nitric oxide/cgmp signaling neuronal nitric oxide nitric oxide synthase pressure overload-induced hypertrophy arginine-depleted cells leading reduced ischemia-reperfusion injury interleukin-1β-converting enzyme cardiac nitric oxide nitric oxide synthases reactive oxygen species peroxynitrite-induced myocardial injury nitric oxide signaling left ventricular function cardiac sarcoplasmic reticulum exogenous nitric oxide cardiac myocyte-specific expression β-adrenergic contractility peroxynitrite-mediated cellular injury myocardial oxygen consumption s-nitrosothiol conserved reactive nitrogen species nitric oxide production nitric oxide regulation von der leyen myofibillar creatine kinase severe cardiac dysfunction high-energy phosphates congestive heart failure privacy choices/manage cookies protein s-nitrosylation cellular biochemistry aims van faassen ee β-adrenergic hyporesponsiveness

Questions {❓}

Mannick JB, Schonhoff CM (2002) Nitrosylation: the next phosphorylation?
Martin SR, Emanuel K, Sears CE et al (2006) Are myocardial eNOS and nNOS involved in the β-adrenergic and muscarinic regulation of inotropy?
Nathan C (1997) Inducible nitric oxide synthase: what difference does it make?
Paulus WJ, Bronzwaer JG (2004) Nitric oxide’s role in the heart: control of beating or breathing?

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         headline:Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart
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      headline:Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart
      description:Nitric oxide (NO) produced in the heart by nitric oxide synthase (NOS) is a highly reactive signaling molecule and an important modulator of myocardial function. NOS catalyzes the conversion of l-arginine to l-citrulline and NO but under particular circumstances reactive oxygen species (ROS) can be formed instead of NO (uncoupling). In the heart, three NOS isoforms are present: neuronal NOS (nNOS, NOS1) and endothelial NOS (eNOS, NOS3) are constitutively present enzymes in distinct subcellular locations within cardiomyocytes, whereas inducible NOS (iNOS, NOS2) is absent in the healthy heart, but its expression is induced by pro-inflammatory mediators. In the tissue, NO has two main effects: (i) NO stimulates the activity of guanylate cyclase, leading to cGMP generation and activation of protein kinase G, and (ii) NO nitrosylates tyrosine and thiol-groups of cysteine in proteins. Upon nitrosylation, proteins may change their properties. Changes in (i) NOS expression and activity, (ii) subcellular compartmentation of NOS activity, and (iii) the occurrence of uncoupling may lead to multiple NO-induced effects, some of which being particularly evident during myocardial overload as occurs during aortic constriction and myocardial infarction. Many of these NO-induced effects are considered to be cardioprotective but particularly if NOS becomes uncoupled, formation of ROS in combination with a low NO bioavailability predisposes for cardiac damage.
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