ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 31 citations in OpenAlex.
- Opposite effects of GαNaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Altered Protein Kinase A-Dependent Phosphorylation of Cav1.2 in Left Ventricular Myocardium fromInternational journal of molecular sciences · 2024Article
- Interaction of the Joining Region in Junctophilin-2 With the L-Type CaCirculation research · 2021Article
- Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies.EBioMedicine · 2020Article
- Degradation of T-Tubular Microdomains and Altered cAMP Compartmentation Lead to Emergence of Arrhythmogenic Triggers in Heart Failure Myocytes: AnFrontiers in physiology · 2018Article
- Microdomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.Circulation research · 2016Article
- Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression.Nature communications · 2016Article
- Phosphorylation sites in the Hook domain of CaVβ subunits differentially modulate CaV1.2 channel function.Journal of molecular and cellular cardiology · 2015Article
- Excitation-contraction coupling of human induced pluripotent stem cell-derived cardiomyocytes.Frontiers in cell and developmental biology · 2015Review
- L-type Ca2+ channel responses to bay k 8644 in stem cell-derived cardiomyocytes are unusually dependent on holding potential and charge carrier.Assay and drug development technologies · 2014Article
- Pyruvate restores β-adrenergic sensitivity of L-type Ca(2+) channels in failing rat heart: role of protein phosphatase.American journal of physiology. Heart and circulatory physiology · 2013Article
- Ahnak1 is a tuneable modulator of cardiac Ca(v)1.2 calcium channel activity.Journal of muscle research and cell motility · 2011Article
- Reverse remodeling with left ventricular assist devices: a review of clinical, cellular, and molecular effects.Circulation. Heart failure · 2011Review
- Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.American journal of physiology. Heart and circulatory physiology · 2010Article
- {beta}1-Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways.American journal of physiology. Heart and circulatory physiology · 2010Article
- GSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in mice.The Journal of clinical investigation · 2010Article
- Transgenic simulation of human heart failure-like L-type Ca2+-channels: implications for fibrosis and heart rate in mice.Cardiovascular research · 2009Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Abnormal L-type Ca(2+) channel (LTCC, also named Cav1.2) density and regulation are important contributors to depressed contractility in failing hearts. The LTCC agonist BAY K 8644 (BAY K) has reduced inotropic effects on failing myocardium. We hypothesized that BAY K effects on the LTCC current (I(CaL)) in failing myocytes would be reduced because of increased basal activity. Since support of the failing heart with a left ventricular assist device (LVAD) improves contractility and adrenergic responses, we further hypothesized that BAY K effects on I(CaL) would be restored in LVAD-supported failing hearts. We tested our hypotheses in human ventricular myocytes (HVMs) isolated from nonfailing (NF), failing (F), and LVAD-supported failing hearts. We found that 1) BAY K had smaller effects on I(CaL) in F HVMs compared with NF HVMs; 2) BAY K had diminished effects on I(CaL) in NF HVM pretreated with isoproterenol (Iso) or dibutyryl cyclic AMP (DBcAMP); 3) BAY K effects on I(CaL) in F HVMs pretreated with acetylcholine (ACh) were normalized; 4) Iso had no effect on NF HVMs pretreated with BAY K; 5) BAY K effects on I(CaL) in LVAD HVMs were similar to those in NF HVMs; 6) BAY K effects were reduced in LVAD HVMs pretreated with Iso or DBcAMP; 7) Iso had no effect on I(CaL) in LVAD HVMs pretreated with BAY K. Collectively, these results suggest that the decreased BAY K effects on LTCC in F HVMs are caused by increased basal channel activity, which should contribute to abnormal contractility reserve.
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Registered trials
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