ArticleThe Journal of physiology2002
The mechanism of the force enhancement by MgADP under simulated ischaemic conditions in rat cardiac myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 46 citations in OpenAlex.
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- Long-Term PDE-5A Inhibition Improves Myofilament Function in Left and Right Ventricular Cardiomyocytes through Partially Different Mechanisms in Diabetic Rat Hearts.Antioxidants (Basel, Switzerland) · 2021Article
- Interventricular Differences of Signaling Pathways-Mediated Regulation of Cardiomyocyte Function in Response to High Oxidative Stress in the Post-Ischemic Failing Rat Heart.Antioxidants (Basel, Switzerland) · 2021Article
- Prophylactic, single-drug cardioprotection in a comparative, experimental study of doxorubicin-induced cardiomyopathy.Journal of translational medicine · 2020Article
- Advantages of prophylactic versus conventionally scheduled heart failure therapy in an experimental model of doxorubicin-induced cardiomyopathy.Journal of translational medicine · 2019Article
- Long Term Osmotic Mini Pump Treatment with Alpha-MSH Improves Myocardial Function in Zucker Diabetic Fatty Rats.Molecules (Basel, Switzerland) · 2017Article
- Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in CaMolecular and cellular biochemistry · 2017Article
- Rapid frequency-dependent changes in free mitochondrial calcium concentration in rat cardiac myocytes.The Journal of physiology · 2017Article
- ADP-stimulated contraction: A predictor of thin-filament activation in cardiac disease.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Synergistic role of ADP and Ca(2+) in diastolic myocardial stiffness.The Journal of physiology · 2015Article
- Hypermuscular mice with mutation in the myostatin gene display altered calcium signalling.The Journal of physiology · 2014Article
- Increased cardiac myocyte PDE5 levels in human and murine pressure overload hypertrophy contribute to adverse LV remodeling.PloS one · 2013Article
- Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure.Basic research in cardiology · 2012Article
- The peroxynitrite evoked contractile depression can be partially reversed by antioxidants in human cardiomyocytes.Journal of cellular and molecular medicine · 2009Article
- Myofilament degradation and dysfunction of human cardiomyocytes in Fabry disease.The American journal of pathology · 2008Article
- No direct effect of creatine phosphate on the cross-bridge cycle in cardiac myofibrils.Pflugers Archiv : European journal of physiology · 2006Article
- A quantitative analysis of cardiac myocyte relaxation: a simulation study.Biophysical journal · 2006Article
- Myosin heavy chain composition and the economy of contraction in healthy and diseased human myocardium.Journal of muscle research and cell motility · 2005Article
- Effects of Ca2+ -sensitizers in permeabilized cardiac myocytes from donor and end-stage failing human hearts.Journal of muscle research and cell motility · 2004Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, the effects of MgADP and/or MgATP on the Ca2+ -dependent and Ca2+ -independent contractile force restoration were determined in order to identify the origin of the tonic force increase (i.e. ischaemic contracture) which develops during advanced stages of ischaemia. Experiments were performed at 15 degrees C during simulated ischaemic conditions in Triton-skinned right ventricular myocytes from rats. In the presence of 5 mM MgATP the maximal Ca2+ -dependent force (P(o)) of 39 +/- 2 kN m(-2) (mean +/- S.E.M.) under control conditions (pH 7.0, 15 mM phosphocreatine (CP)) decreased to 8 +/- 1 % during simulated ischaemia (pH 6.2, 30 mM inorganic phosphate (P(i)), without CP). This change was accompanied by a major reduction in Ca2+ sensitivity (pCa(50) 4.10 vs. 5.62). Substitution of MgADP for MgATP restored isometric force production and its Ca2+ sensitivity (pCa(50) 4.74 at 4 mM MgADP and 1 mM MgATP). In addition, it shifted the MgATP threshold concentration of Ca2+ -independent force development to higher levels in a concentration-dependent manner. However, Ca2+ -independent force was facilitated less by MgADP than Ca2+ -dependent force. The MgADP-induced increase in force was accompanied by marked reductions in the velocity of unloaded shortening and the rate of tension redevelopment. These data and simulations using a model of cross-bridge kinetics suggest that the ischaemic force is not a consequence of a reduction in intracellular MgATP concentration, but identify MgADP as a key modulator of the cross-bridge cycle under simulated ischaemic conditions in cardiac muscle, with a much lower inhibition constant (0.012 +/- 0.003 mM) than in skeletal muscle. Therefore, MgADP has a high potential to stabilize the force-generating cross-bridge state and to facilitate the development of ischaemic contracture, possibly involving a Ca2+ activation process in the ischaemic myocardium.
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