ArticleThe Journal of clinical investigation2000
beta(3)-adrenoceptor deficiency blocks nitric oxide-dependent inhibition of myocardial contractility.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 128 citations in OpenAlex.
- Potential roles of β3-adrenergic receptor in heart rate regulation via sinus node activity and local adipocyte metabolism.The journal of physiological sciences : JPS · 2026Article
- Adrenoceptor Desensitization: Current Understanding of Mechanisms.Pharmacological reviews · 2024Review
- Efficacy of a growth hormone-releasing hormone agonist in a murine model of cardiometabolic heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023Article
- Pathophysiology and pharmacology of G protein-coupled receptors in the heart.Cardiovascular research · 2023Review
- Synthetic growth hormone-releasing hormone agonist ameliorates the myocardial pathophysiology characteristic of heart failure with preserved ejection fraction.Cardiovascular research · 2023Article
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- Growth hormone-releasing hormone agonists ameliorate chronic kidney disease-induced heart failure with preserved ejection fraction.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- Healthful aging mediated by inhibition of oxidative stress.Ageing research reviews · 2020Review
- Selective activation of GMolecular metabolism · 2019Article
- Spotlight on ROS andOxidative medicine and cellular longevity · 2019Review
- Alterations of tumor microenvironment by nitric oxide impedes castration-resistant prostate cancer growth.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Nitric oxide signalling in cardiovascular health and disease.Nature reviews. Cardiology · 2018Review
- Aerobic exercise protects against pressure overload-induced cardiac dysfunction and hypertrophy via β3-AR-nNOS-NO activation.PloS one · 2017Article
- Transcriptomic Analysis Identifies the Effect of Beta-Blocking Agents on a Molecular Pathway of Contraction in the Heart and Predicts Response to Therapy.JACC. Basic to translational science · 2016Review
- A pathway and network review on beta-adrenoceptor signaling and beta blockers in cardiac remodeling.Heart failure reviews · 2014Review
- β3-Adrenoreceptor stimulation protects against myocardial infarction injury via eNOS and nNOS activation.PloS one · 2014Article
- Nebivolol protects against myocardial infarction injury via stimulation of beta 3-adrenergic receptors and nitric oxide signaling.PloS one · 2014Article
- miR-222 contributes to sex-dimorphic cardiac eNOS expression via ets-1.Physiological genomics · 2013Article
- Alagebrium in combination with exercise ameliorates age-associated ventricular and vascular stiffness.Experimental gerontology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The cardiac beta-adrenergic pathway potently stimulates myocardial performance, thereby providing a mechanism for myocardial contractile reserve. beta-Adrenergic activation also increases cardiac nitric oxide (NO) production, which attenuates positive inotropy, suggesting a possible negative feedback mechanism. Recently, in vitro studies suggest that stimulation of the beta(3)-adrenoceptor results in a negative inotropic effect through NO signaling. In this study, using mice with homozygous beta(3)-adrenoceptor deletion mutations, we tested the hypothesis that the beta(3)-adrenoceptor is responsible for beta-adrenergic activation of NO. Although resting indices of myocardial contraction were similar, beta-adrenergic-stimulated inotropy was increased in beta(3)(-/-) mice, and similar hyper-responsiveness was seen in mice lacking endothelial NO synthase (NOS3). NOS inhibition augmented isoproterenol-stimulated inotropy in wild-type (WT), but not in beta(3)(-/-) mice. Moreover, isoproterenol increased myocardial cGMP in WT, but not beta(3)(-/-), mice. NOS3 protein abundance was not changed in beta(3)(-/-) mice, and cardiac beta(3)-adrenoceptor mRNA was detected in both NOS3(-/-) and WT mice. These findings indicate that the beta(3)-adrenergic subtype participates in NO-mediated negative feedback over beta-adrenergic stimulation.
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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.