ReviewThe Journal of physiology2003
Modulation of cardiac contraction, relaxation and rate by the endothelial nitric oxide synthase (eNOS): lessons from genetically modified mice.
Review in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 160 citations in OpenAlex.
- Impact of Bilateral and Single Internal Thoracic Artery Bypass Grafting on Postoperative Reverse Remodeling in Patients with End-Stage Ischemic Cardiomyopathy.Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia · 2026Article
- Modeling the interplay of sex hormones in cardiac hypertrophic signaling.PLoS computational biology · 2025Article
- Mechanotransduction-Driven Modulation ofInternational journal of molecular sciences · 2025Article
- NONO2P, a nitric oxide donor, induces relaxation in coronary artery, negative inotropism and hypotensive effect in rats.Biochemical pharmacology · 2025Article
- CCL2-mediated endothelial injury drives cardiac dysfunction in long COVID.Nature cardiovascular research · 2024Article
- Modulating NO-GC Pathway in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- Endothelial-derived extracellular vesicles from obese/hypertensive adults increase factors associated with hypertrophy and fibrosis in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2023Article
- Nitric Oxide in Cardiac Surgery: A Review Article.Biomedicines · 2023Review
- Red blood cell eNOS is cardioprotective in acute myocardial infarction.Redox biology · 2022Article
- Oral administration of TiOParticle and fibre toxicology · 2022Article
- A Review on the Role of TRP Channels and Their Potential as Drug Targets_An Insight Into the TRP Channel Drug Discovery Methodologies.Frontiers in pharmacology · 2022Review
- Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States.American journal of biomedical science & research · 2022Article
- Cardiomyocyte depolarization triggers NOS-dependent NO transient after calcium release, reducing the subsequent calcium transient.Basic research in cardiology · 2021Article
- Nitric Oxide and S-Nitrosylation in Cardiac Regulation: G Protein-Coupled Receptor Kinase-2 and β-Arrestins as Targets.International journal of molecular sciences · 2021Review
- The Dipeptidyl Peptidase-4 Inhibitor Linagliptin Directly Enhances the Contractile Recovery of Mouse Hearts at a Concentration Equivalent to that Achieved with Standard Dosing in Humans.International journal of molecular sciences · 2020Article
- Blood pressure-lowering effects of a Bowman-Birk inhibitor and its derived peptides in normotensive and hypertensive rats.Scientific reports · 2020Article
- Identifying modifier genes for hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology · 2020Article
- Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease.PLoS pathogens · 2020Article
- Advantages of Phosphodiesterase Type 5 Inhibitors in the Management of Glucose Metabolism Disorders: A Clinical and Translational Issue.International journal of endocrinology · 2020Review
- Neuronal NO synthase mediates plenylephrine induced cardiomyocyte hypertrophy through facilitation of NFAT-dependent transcriptional activity.Biochemistry and biophysics reports · 2019Article
1 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The modulatory role of endothelial nitric oxide synthase (eNOS) on heart contraction, relaxation and rate is examined in light of recent studies using genetic deletion or overexpression in mice under specific conditions. Unstressed eNOS-/- hearts in basal conditions exhibit a normal inotropic and lusitropic function, with either decreased or unchanged heart rate. Under stimulation with catecholamines, eNOS-/- mice predominantly show a potentiation in their beta-adrenergic inotropic and lusitropic responsiveness. A similar phenotype is observed in beta 3-adrenoceptor deficient mice, pointing to a key role of this receptor subtype for eNOS coupling. The effect of eNOS on the muscarinic cholinergic modulation of cardiac function probably operates in conjunction with other NO-independent mechanisms, the persistence of which may explain the apparent dispensability of this isoform for the effect of acetylcholine in some eNOS-/- mouse strains. eNOS-/- hearts submitted to short term ischaemia-reperfusion exhibit variable alterations in systolic and diastolic function and infarct size, while those submitted to myocardial infarction present a worsened ventricular remodelling, increased 1 month mortality and loss of benefit from ACE inhibitor or angiotensin II type I receptor antagonist therapy. Although non-conditional eNOS gene deletion may engender phenotypic adaptations (e.g. ventricular hypertrophy resulting from chronic hypertension, or upregulation of the other NOS isoforms) potentially confounding the interpretation of comparative studies, the use of eNOS-/- mice has undoubtedly advanced (and will probably continue to improve) our understanding of the complex role of eNOS (in conjunction with the other NOSs) in the regulation of cardiac function. The challenge is now to confirm the emerging paradigms in human cardiac physiology and hopefully translate them into therapy.
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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.