Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats

G. Szigeti, János Almássy, Mónika Sztretye, Beatrix Dienes, László Szabó, P. Szentesi, Guy Vassort, S. Sárközi, L. Csernoch, I. Jóna

Research output: Contribution to journalArticle

7 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)541-553
Number of pages13
JournalPflugers Archiv European Journal of Physiology
Volume455
Issue number3
DOIs
Publication statusPublished - Dec 2007

Fingerprint

Muscle
Rats
Skeletal Muscle
Homeostasis
Calcium
Ryanodine Receptor Calcium Release Channel
Electric potential
Myocardial Infarction
Excitation Contraction Coupling
Calcium Signaling
Coronary Occlusion
Skeletal Muscle Fibers
Sarcoplasmic Reticulum
Calcium Channels
Coronary Vessels
Electric sparks
Heart Failure
Animals
Chemical activation
Fibers

Keywords

  • Calcium sparks
  • Calcium transients
  • Charge movement
  • Myocardial infarction
  • Ryanodine receptor
  • Single channel

ASJC Scopus subject areas

  • Physiology

Cite this

Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats. / Szigeti, G.; Almássy, János; Sztretye, Mónika; Dienes, Beatrix; Szabó, László; Szentesi, P.; Vassort, Guy; Sárközi, S.; Csernoch, L.; Jóna, I.

In: Pflugers Archiv European Journal of Physiology, Vol. 455, No. 3, 12.2007, p. 541-553.

Research output: Contribution to journalArticle

Szigeti, G. ; Almássy, János ; Sztretye, Mónika ; Dienes, Beatrix ; Szabó, László ; Szentesi, P. ; Vassort, Guy ; Sárközi, S. ; Csernoch, L. ; Jóna, I. / Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats. In: Pflugers Archiv European Journal of Physiology. 2007 ; Vol. 455, No. 3. pp. 541-553.
@article{6f19590541804c0592bd1315584ca0ff,
title = "Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats",
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.",
keywords = "Calcium sparks, Calcium transients, Charge movement, Myocardial infarction, Ryanodine receptor, Single channel",
author = "G. Szigeti and J{\'a}nos Alm{\'a}ssy and M{\'o}nika Sztretye and Beatrix Dienes and L{\'a}szl{\'o} Szab{\'o} and P. Szentesi and Guy Vassort and S. S{\'a}rk{\"o}zi and L. Csernoch and I. J{\'o}na",
year = "2007",
month = "12",
doi = "10.1007/s00424-007-0298-z",
language = "English",
volume = "455",
pages = "541--553",
journal = "Pflugers Archiv European Journal of Physiology",
issn = "0031-6768",
publisher = "Springer Verlag",
number = "3",

}

TY - JOUR

T1 - Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats

AU - Szigeti, G.

AU - Almássy, János

AU - Sztretye, Mónika

AU - Dienes, Beatrix

AU - Szabó, László

AU - Szentesi, P.

AU - Vassort, Guy

AU - Sárközi, S.

AU - Csernoch, L.

AU - Jóna, I.

PY - 2007/12

Y1 - 2007/12

N2 - 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.

AB - 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.

KW - Calcium sparks

KW - Calcium transients

KW - Charge movement

KW - Myocardial infarction

KW - Ryanodine receptor

KW - Single channel

UR - http://www.scopus.com/inward/record.url?scp=35448963860&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35448963860&partnerID=8YFLogxK

U2 - 10.1007/s00424-007-0298-z

DO - 10.1007/s00424-007-0298-z

M3 - Article

C2 - 17558517

AN - SCOPUS:35448963860

VL - 455

SP - 541

EP - 553

JO - Pflugers Archiv European Journal of Physiology

JF - Pflugers Archiv European Journal of Physiology

SN - 0031-6768

IS - 3

ER -