ReviewNaunyn-Schmiedeberg's archives of pharmacology2007
Beta-adrenoceptor blocker treatment and the cardiac beta-adrenoceptor-G-protein(s)-adenylyl cyclase system in chronic heart failure.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 68 citations in OpenAlex.
- The identification of adenylyl cyclase modulators as potential receptors for 6-nitrodopamine in human-induced pluripotent stem cell (hiPSC)-derived cardiomyocytes and their relevance in heart inotropism.Frontiers in pharmacology · 2025Article
- 3-Nitroatenolol: First Synthesis, Chiral Resolution and Enantiomers' Absolute Configuration.Molecules (Basel, Switzerland) · 2024Article
- Unveiling Switching Function of Amino Acids in Proteins Using a Machine Learning Approach.Journal of chemical theory and computation · 2023Article
- Handling of Ventricular Fibrillation in the Emergency Setting.Frontiers in pharmacology · 2019Review
- Article
- Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance.Antioxidants & redox signaling · 2014Review
- let-7e replacement yields potent anti-arrhythmic efficacy via targeting beta 1-adrenergic receptor in rat heart.Journal of cellular and molecular medicine · 2014Article
- Pharmacogenomics of cardiovascular complications in diabetes and obesity.Recent patents on biotechnology · 2014Review
- Targeting GRK2 by gene therapy for heart failure: benefits above β-blockade.Gene therapy · 2012Review
- Chronic sympathetic activation promotes downregulation of β-adrenoceptor-mediated effects in the guinea pig heart independently of structural remodeling and systolic dysfunction.Pflugers Archiv : European journal of physiology · 2011Article
- Cardiac disease in mucopolysaccharidosis type I attributed to catecholaminergic and hemodynamic deficiencies.American journal of physiology. Heart and circulatory physiology · 2011Article
- Tissue functions mediated by beta(3)-adrenoceptors-findings and challenges.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Mechanisms of pharmacogenomic effects of genetic variation within the cardiac adrenergic network in heart failure.Molecular pharmacology · 2009Review
- Beta 1- and beta 2-adrenoceptor polymorphisms and cardiovascular diseases.British journal of pharmacology · 2009Review
- Decreased beta-adrenergic responsiveness following hypertrophy occurs only in cardiomyocytes that also re-express beta-myosin heavy chain.European journal of heart failure · 2009Article
- Lack of specificity of antibodies directed against human beta-adrenergic receptors.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Modulation of rat parasympathetic cardiac ganglion phenotype and NGF synthesis by adrenergic nerves.Autonomic neuroscience : basic & clinical · 2009Article
- Sildenafil stops progressive chamber, cellular, and molecular remodeling and improves calcium handling and function in hearts with pre-existing advanced hypertrophy caused by pressure overload.Journal of the American College of Cardiology · 2009Article
- Ventricular arrhythmias after left ventricular assist device implantation.Pacing and clinical electrophysiology : PACE · 2008Article
- Activator of G protein signaling 3 null mice: I. Unexpected alterations in metabolic and cardiovascular function.Endocrinology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies showed that chronic beta-adrenoceptor (AR) blocker treatment exerts beneficial effects in patients with chronic heart failure (CHF). In CHF, sympathetic drive to the heart is increased, and this causes pathological changes in cardiac beta-AR-G-protein(s)-adenylyl cyclase system: Cardiac beta-1 AR are decreased, and amount and activity of cardiac G(i)-protein and G-protein-coupled receptor kinase (GRK) are increased resulting in diminished cardiac beta-AR functional responsiveness. One possible mechanism of beneficial effects of beta-AR blockers could be that they prevent adverse effects of increased sympathetic activity and up-regulate cardiac (and vascular) beta-AR density, and by this, enhance beta-AR-mediated effects. Another possibility could be that chronic beta-AR blocker treatment normalizes activity of G(i)-protein and may thereby restore beta-AR functional responsiveness. Moreover, failing human heart exhibits an inverse force-frequency relationship. beta-AR blockers reduce heart rate; this may, therefore, improve force of contraction. One of the strongest stimuli to activate GRK is increased sympathetic activity (as in CHF) via beta-AR stimulation. beta-AR blockers, by blocking beta-AR, can prevent GRK activation and/or can reduce the (previously enhanced) GRK activity, and this might-at least partly-contribute to beneficial effects of beta-AR blockers in CHF treatment. Finally, the "loss-of-function" Arg389Gly beta-1 AR polymorphism seems to determine heart rate and blood pressure responses to beta-1 AR blocker administration: Arg389Arg beta-1 AR subjects exhibit stronger effects than subjects with one or two Gly389 alleles. Thus, it might be predicted that patients homozygous Arg389 beta-1 AR should be good responders, whereas patients homozygous Gly389 beta-1 AR polymorphism should be poor or non-responders.
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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.