ArticleJournal of cellular and molecular medicine2011
β-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodelling in congestive heart failure.
Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Topical Anti-ulcerogenic Effect of the Beta-adrenergic Blockers on Diabetic Foot Ulcers: Recent Advances and Future Prospectives.Current diabetes reviews · 2024Review
- Beta-Blockers and Their Current Role in Maternal and Neonatal Health: A Narrative Review of the Literature.Cureus · 2023Review
- Medication and ECG Patterns That May Hinder SPECT Myocardial Perfusion Scans.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Heart Failure with Improved Ejection Fraction: Insight into the Variable Nature of Left Ventricular Systolic Function.International journal of environmental research and public health · 2022Review
- Proteomics of acute heart failure in a rat post-myocardial infarction model.Molecular medicine reports · 2017Article
- A Potential Link between the C5a Receptor 1 and the β1-Adrenoreceptor in the Mouse Heart.PloS one · 2016Article
- Small and large animal models in cardiac contraction research: advantages and disadvantages.Pharmacology & therapeutics · 2014Review
- The action of p-synephrine on hepatic carbohydrate metabolism and respiration occurs via both Ca(2+)-mobilization and cAMP production.Molecular and cellular biochemistry · 2014Article
- Adrenergic metabolic and hemodynamic effects of octopamine in the liver.International journal of molecular sciences · 2013Article
- Reversal of subcellular remodelling by losartan in heart failure due to myocardial infarction.Journal of cellular and molecular medicine · 2012Article
- Cardiac remodeling and subcellular defects in heart failure due to myocardial infarction and aging.Heart failure reviews · 2012Review
- Role of various proteases in cardiac remodeling and progression of heart failure.Heart failure reviews · 2012Review
- Mechanisms of the beneficial effects of beta-adrenoceptor antagonists in congestive heart failure.Experimental and clinical cardiology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although β-adrenoceptor (β-AR) blockade is an important mode of therapy for congestive heart failure (CHF), subcellular mechanisms associated with its beneficial effects are not clear. Three weeks after inducing myocardial infarction (MI), rats were treated daily with or without 20 and 75 mg/kg atenolol, a selective β(1) -AR antagonist, or propranolol, a non-selective β-AR antagonist, for 5 weeks. Sham operated rats served as controls. All animals were assessed haemodynamically and echocardiographically and the left ventricle (LV) was processed for the determination of myofibrillar ATPase activity, α- and β-myosin heavy chain (MHC) isoforms and gene expression as well as cardiac troponin I (cTnI) phosphorylation. Both atenolol and propranolol at 20 and 75 mg/kg doses attenuated cardiac hypertrophy and lung congestion in addition to increasing LV ejection fraction and LV systolic pressure as well as decreasing heart rate, LV end-diastolic pressure and LV diameters in the infarcted animals. Treatment of infarcted animals with these agents also attenuated the MI-induced depression in myofibrillar Ca(2+) -stimulated ATPase activity and phosphorylated cTnI protein content. The MI-induced decrease in α-MHC and increase in β-MHC protein content were attenuated by both atenolol and propranolol at low and high doses; however, only high dose of propranolol was effective in mitigating changes in the gene expression for α-MHC and β-MHC. Our results suggest that improvement of cardiac function by β-AR blockade in CHF may be associated with attenuation of myofibrillar remodelling.
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Registered trials
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