ArticleThe Journal of physiology2004
Essential role of troponin I in the positive inotropic response to isoprenaline in mouse hearts contracting auxotonically.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Loss of phospholamban phosphorylation blunts CaJournal of molecular and cellular cardiology · 2026Article
- Arg92Leu-cTnT Alters the cTnC-cTnI Interface Disrupting PKA-Mediated Relaxation.Circulation research · 2024Article
- Alterations of sarcoplasmic reticulum-mediated CaMolecular and cellular biochemistry · 2023Article
- Cardiac deficiency of P21-activated kinase 1 promotes atrial arrhythmogenesis in mice following adrenergic challenge.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- Loss of autophagy protein ATG5 impairs cardiac capacity in mice and humans through diminishing mitochondrial abundance and disrupting Ca2+ cycling.Cardiovascular research · 2022Article
- Suppression of lusitropy as a disease mechanism in cardiomyopathies.Frontiers in cardiovascular medicine · 2022Review
- Quantitative Analysis of the Cardiac Phosphoproteome in Response to Acute β-Adrenergic Receptor Stimulation In Vivo.International journal of molecular sciences · 2021Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- Functional analysis of a gene-edited mouse model to gain insights into the disease mechanisms of a titin missense variant.Basic research in cardiology · 2021Article
- Monophosphorylation of cardiac troponin-I at Ser-23/24 is sufficient to regulate cardiac myofibrillar CaThe Journal of biological chemistry · 2018Article
- TRPA1 ion channel stimulation enhances cardiomyocyte contractile function via a CaMKII-dependent pathway.Channels (Austin, Tex.) · 2017Article
- Omecamtiv Mecarbil Abolishes Length-Mediated Increase in Guinea Pig Cardiac Myofiber CaBiophysical journal · 2017Article
- Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling.Scientific reports · 2016Article
- The contributions of cardiac myosin binding protein C and troponin I phosphorylation to β-adrenergic enhancement of in vivo cardiac function.The Journal of physiology · 2016Article
- Cardiac Myosin Binding Protein-C Phosphorylation Modulates Myofilament Length-Dependent Activation.Frontiers in physiology · 2016Article
- Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.Cardiovascular research · 2015Article
- Alpha1 catalytic subunit of AMPK modulates contractile function of cardiomyocytes through phosphorylation of troponin I.Life sciences · 2014Article
- p38α regulates SERCA2a function.Journal of molecular and cellular cardiology · 2014Article
- Ceramide-mediated depression in cardiomyocyte contractility through PKC activation and modulation of myofilament protein phosphorylation.Basic research in cardiology · 2014Article
- Length dependence of striated muscle force generation is controlled by phosphorylation of cTnI at serines 23/24.The Journal of physiology · 2013Article
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Authors and funding
6 authors.
Funding
Abstract
PKA-dependent phosphorylation of cardiac troponin I (cTnI) contributes significantly to beta-adrenergic agonist-induced acceleration of myocardial relaxation (lusitropy). However, the role of PKA-dependent cTnI phosphorylation in the positive inotropic response to beta-adrenergic stimulation is unclear. We studied the contractile response to isoprenaline (10 nm) in isolated hearts and isolated cardiomyocytes from transgenic mice with cardiac-specific expression of slow skeletal TnI (ssTnI, which lacks the N-terminal protein extension containing PKA-sensitive phosphorylation sites in cTnI) and matched wild-type littermate controls. As expected, the lusitropic effect of isoprenaline was significantly blunted in ssTnI hearts. However, the positive inotropic response to isoprenaline was also blunted in ssTnI hearts. This effect was especially prominent for ejection-phase indices in isolated auxotonically loaded ssTnI hearts whereas the positive inotropic response of isovolumic hearts or unloaded isolated myocytes was much less affected. Isoprenaline decreased left ventricular end-systolic volume in wild-type hearts (10.6 +/- 1.6 to 6.2 +/- 0.4 microl at a preload of 20 cmH(2)O; P < 0.05) but not transgenic hearts (11.4 +/- 1.3 to 10.9 +/- 1.3 microl; P= n.s.). Likewise, isoprenaline increased stroke work in control hearts (14.5 +/- 1.0 to 22.5 +/- 1.8 mmHg microl mg(-1); P < 0.05) but not transgenic hearts (15.4 +/- 1.3 to 18.3 +/- 1.2 mmHg microl mg(-1); P= n.s.). The end-systolic pressure-volume relation was increased by isoprenaline to a greater extent in control than transgenic hearts. However, isoprenaline induced a similar rise in intracellular Ca(2+) transients in transgenic and non-transgenic cardiomyocytes. These results indicate that cTnI has a pivotal role in the positive inotropic response of the murine heart to beta-adrenergic stimulation, an effect that is highly dependent on loading conditions and is most evident in the auxotonically loaded ejecting heart.
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