ArticlePflugers Archiv : European journal of physiology2007
Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- EuBiophysical journal · 2023Article
- Function of a mutant ryanodine receptor (T4709M) linked to congenital myopathy.Scientific reports · 2023Article
- Lanthanides Report Calcium Sensor in the Vestibule of Ryanodine Receptor.Biophysical journal · 2017Article
- Effects of K-201 on the calcium pump and calcium release channel of rat skeletal muscle.Pflugers Archiv : European journal of physiology · 2008Article
- Stressed out: the skeletal muscle ryanodine receptor as a target of stress.The Journal of clinical investigation · 2008Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic heart failure, skeletal muscles develop a weakness that is not associated to an impaired circulatory function but rather to alterations in the skeletal muscle fibers themselves. To understand these changes, the steps in excitation-contraction coupling of rats that underwent a left anterior coronary artery occlusion were studied. About 24 weeks after the myocardial infarction, neither the total amount nor the voltage dependence of intramembrane charge were altered. In contrast, calcium release from the sarcoplasmic reticulum was considerably suppressed, and its voltage dependence shifted toward more positive voltages. Elementary calcium-release events showed altered morphology as the relative proportion of embers increased. Calcium sparks were smaller in amplitude and had larger time-to-peak values. Isolated ryanodine receptors (RyR) displayed an unusual rectification with increased single-channel conductance at positive (cis vs trans) voltages. In addition, the bell-shaped calcium dependence of channel activity was broader, with a slight shift of activation to lower and a larger shift in inactivation to higher calcium concentrations. These data indicate that the number of channels that open during a calcium-release event is decreased and that RyR function is altered; thus, calcium-release is suppressed after a myocardial infarction. These observations give an explanation for the impaired skeletal muscle function in these animals.
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