ArticleAmerican journal of physiology. Cell physiology2008
Neuronal nitric oxide synthase signaling within cardiac myocytes targets phospholamban.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- Chamber-specific regulation of myofilament Ca2+ sensitivity by nNOSβ via troponin I phosphorylation: Predominance in the right ventricle.The Journal of general physiology · 2026Article
- Effects of arginase inhibition on myocardial CaPhysiological reports · 2022Article
- Review
- 'Social distancing' of the neuronal nitric oxide synthase from its adaptor protein causes arrhythmogenic trigger-substrate interactions in long QT syndrome.Cardiovascular research · 2021Article
- Sex Differences in Cardiovascular Aging and Heart Failure.Current heart failure reports · 2020Review
- Enhanced dimethylarginine degradation improves coronary flow reserve and exercise tolerance in Duchenne muscular dystrophy carrier mice.American journal of physiology. Heart and circulatory physiology · 2020Article
- An emerging perspective on sex differences: Intersecting S-nitrosothiol and aldehyde signaling in the heart.Redox biology · 2020Review
- An enhanced expression of hypothalamic neuronal nitric oxide synthase in a rat model of simulated transport stress.BMC veterinary research · 2019Article
- Article
- The Subcellular Localisation of Neuronal Nitric Oxide Synthase Determines the Downstream Effects of NO on Myocardial Function.Cardiovascular research · 2017Article
- Acute ascorbic acid infusion increases left ventricular diastolic function in postmenopausal women.Maturitas · 2016Article
- Ischemic postconditioning protects the heart against ischemia-reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria.Cell death & disease · 2016Article
- Article
- S-Nitrosylation of Calcium-Handling Proteins in Cardiac Adrenergic Signaling and Hypertrophy.Circulation research · 2015Article
- Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect.Journal of visualized experiments : JoVE · 2015Article
- Current understanding of molecular pathology and treatment of cardiomyopathy in duchenne muscular dystrophy.Molecules (Basel, Switzerland) · 2015Review
- Obligatory role of neuronal nitric oxide synthase in the heart's antioxidant adaptation with exercise.Journal of molecular and cellular cardiology · 2015Article
- Tri-modal regulation of cardiac muscle relaxation; intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.Biophysical reviews · 2014Article
- Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance.Antioxidants & redox signaling · 2014Review
- NADPH oxidase-2 inhibition restores contractility and intracellular calcium handling and reduces arrhythmogenicity in dystrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2014Article
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6 authors at 1 institution in 1 country.
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Abstract
Studies have shown that neuronal nitric oxide synthase (nNOS, NOS1) knockout mice (NOS1-/-) have increased or decreased contractility, but consistently have found a slowed rate of intracellular Ca2+ ([Ca2+]i) decline and relengthening. Contraction and [Ca2+]i decline are determined by many factors, one of which is phospholamban (PLB). The purpose of this study is to determine the involvement of PLB in the NOS1-mediated effects. Force-frequency experiments were performed in trabeculae isolated from NOS1-/- and wild-type (WT) mice. We also simultaneously measured Ca2+ transients (Fluo-4) and cell shortening (edge detection) in myocytes isolated from WT, NOS1-/-, and PLB-/- mice. NOS1-/- trabeculae had a blunted force-frequency response and prolonged relaxation. We observed similar effects in myocytes with NOS1 knockout or specific NOS1 inhibition with S-methyl-l-thiocitrulline (SMLT) in WT myocytes (i.e., decreased Ca2+ transient and cell shortening amplitudes and prolonged decline of [Ca2+]i). Alternatively, NOS1 inhibition with SMLT in PLB-/- myocytes had no effect. Acute inhibition of NOS1 with SMLT in WT myocytes also decreased basal PLB serine16 phosphorylation. Furthermore, there was a decreased SR Ca2+ load with NOS1 knockout or inhibition, which is consistent with the negative contractile effects. Perfusion with FeTPPS (peroxynitrite decomposition catalyst) mimicked the effects of NOS1 knockout or inhibition. beta-Adrenergic stimulation restored the slowed [Ca2+]i decline in NOS1-/- myocytes, but a blunted contraction remained, suggesting additional protein target(s). In summary, NOS1 inhibition or knockout leads to decreased contraction and slowed [Ca2+]i decline, and this effect is absent in PLB-/- myocytes. Thus NOS1 signaling modulates PLB serine16 phosphorylation, in part, via peroxynitrite.
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