ArticleThe Journal of physiology2010
Regulation of myocyte contraction via neuronal nitric oxide synthase: role of ryanodine receptor S-nitrosylation.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 90 citations in OpenAlex.
- Sex differences in mitochondrial CaJournal of molecular and cellular cardiology · 2026Article
- Regulatory effects of resveratrol on nitric oxide signaling in cardiovascular diseases.Pharmacological reports : PR · 2025Review
- Adipokines as Cardioprotective Factors: BAT Steps Up to the Plate.Biomedicines · 2025Review
- S-nitrosylation of cardiac myocyte proteins may underlie sex differences in cardiac disease.Frontiers in physiology · 2025Review
- Aging mechanism for improving the tenderness and taste characteristics of meat.Journal of animal science and technology · 2023Review
- Review
- Integrative Analyses Identify Potential Key Genes and Calcium-Signaling Pathway in Familial Atrioventricular Nodal Reentrant Tachycardia Using Whole-Exome Sequencing.Frontiers in cardiovascular medicine · 2022Article
- Nitrosative Stress and Human Disease: Therapeutic Potential of Denitrosylation.International journal of molecular sciences · 2021Review
- A Novel Endocrine Role for the BAT-Released Lipokine 12,13-diHOME to Mediate Cardiac Function.Circulation · 2021Article
- Understanding How Phosphorylation and Redox Modifications Regulate Cardiac Ryanodine Receptor Type 2 Activity to Produce an Arrhythmogenic Phenotype in Advanced Heart Failure.ACS pharmacology & translational science · 2020Review
- An emerging perspective on sex differences: Intersecting S-nitrosothiol and aldehyde signaling in the heart.Redox biology · 2020Review
- Nitric Oxide and Mechano-Electrical Transduction in Cardiomyocytes.Frontiers in physiology · 2020Review
- Nitric oxide signalling in cardiovascular health and disease.Nature reviews. Cardiology · 2018Review
- Atrial Infarction-Induced Spontaneous Focal Discharges and Atrial Fibrillation in Sheep: Role of Dantrolene-Sensitive Aberrant Ryanodine Receptor Calcium Release.Circulation. Arrhythmia and electrophysiology · 2018Article
- Redox Dependent Modifications of Ryanodine Receptor: Basic Mechanisms and Implications in Heart Diseases.Frontiers in physiology · 2018Review
- Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium.Frontiers in physiology · 2018Review
- Article
- The Subcellular Localisation of Neuronal Nitric Oxide Synthase Determines the Downstream Effects of NO on Myocardial Function.Cardiovascular research · 2017Article
- Nitric oxide signalling and neuronal nitric oxide synthase in the heart under stress.F1000Research · 2017Review
- The Relationship between Estrogen and Nitric Oxide in the Prevention of Cardiac and Vascular Anomalies in the Developing Zebrafish (Danio Rerio).Brain sciences · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The sarcoplasmic reticulum (SR) Ca(2+) release channel (ryanodine receptor, RyR2) has been proposed to be an end target of neuronal nitric oxide synthase (NOS1) signalling. The purpose of this study is to investigate the mechanism of NOS1 modulation of RyR2 activity and the corresponding effect on myocyte function. Myocytes were isolated from NOS1 knockout (NOS1(/)) and wild-type mice. NOS1(/) myocytes displayed a decreased fractional SR Ca(2+) release, NOS1 knockout also led to reduced RyR2 S-nitrosylation levels. RyR2 channels from NOS1(/) hearts had decreased RyR2 open probability. Additionally, knockout of NOS1 led to a decrease in [(3)H]ryanodine binding, Ca(2+) spark frequency (CaSpF) and a rightward shift in the SR Ca(2+) leak/load relationship. Similar effects were observed with acute inhibition of NOS1. These data are indicative of decreased RyR2 activity in myocytes with NOS1 knockout or acute inhibition. Interestingly, the NO donor and nitrosylating agent SNAP reversed the depressed RyR2 open probability, the reduced CaSpF, and caused a leftward shift in the leak/load relationship in NOS1(/) myocytes. SNAP also normalized Ca(2+) transient and cell shortening amplitudes and SR fractional release in myocytes with NOS1 knockout or acute inhibition. Furthermore, SNAP was able to normalize the RyR2 S-nitrosylation levels. These data suggest that NOS1 signalling increases RyR2 activity via S-nitrosylation, which contributes to the NOS1-induced positive inotropic effect. Thus, RyR2 is an important end target of NOS1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.