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Journal articles on the topic 'Excitation-contraction coupling'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Wann, Samuel. "Contraction–excitation coupling?" Heart Rhythm 9, no. 1 (2012): 91. http://dx.doi.org/10.1016/j.hrthm.2011.08.030.

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2

Bers, Donald M. "Cardiac excitation–contraction coupling." Nature 415, no. 6868 (2002): 198–205. http://dx.doi.org/10.1038/415198a.

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3

Hamilton, Susan L., Irina Serysheva, and Gale M. Strasburg. "Calmodulin and Excitation-Contraction Coupling." Physiology 15, no. 6 (2000): 281–84. http://dx.doi.org/10.1152/physiologyonline.2000.15.6.281.

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Excitation-contraction coupling in cardiac and skeletal muscle involves the transverse-tubule voltage-dependent Ca2+ channel and the sarcoplasmic reticulum Ca2+ release channel. Both of these ion channels bind and are modulated by calmodulin in both its Ca2+-bound and Ca2+-free forms. Calmodulin is, therefore, potentially an important regulator of excitation-contraction coupling. Its precise role, however, has not yet been defined.

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4

Kilfoil, Peter, Xin Yue, Rui Zhang, et al. "Excitation-Contraction Coupling in HFpEF." Biophysical Journal 114, no. 3 (2018): 291a. http://dx.doi.org/10.1016/j.bpj.2017.11.1664.

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5

HAMADA, Tomoyo, Hiromi TERAMI, and Hiroaki KAGAWA. "Excitation-Contraction Coupling in Caenorhabditis elegans." Seibutsu Butsuri 40, no. 1 (2000): 13–19. http://dx.doi.org/10.2142/biophys.40.13.

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6

Marty, Isabelle, and Julien Fauré. "Excitation-Contraction Coupling Alterations in Myopathies." Journal of Neuromuscular Diseases 3, no. 4 (2016): 443–53. http://dx.doi.org/10.3233/jnd-160172.

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7

Marban, E. "Excitation-contraction coupling in hibernating myocardium." Basic Research in Cardiology 90, no. 1 (1995): 19–22. http://dx.doi.org/10.1007/bf00795110.

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8

Khairallah, Philip A., Mary K. Upsher, Kazunari Yoshida, Fetnat M. Fouad, and Mary K. Hanna. "Excitation-Contraction Coupling in Hypertrophied Myocardium." Journal of Cardiovascular Pharmacology 7 (1985): S13—S19. http://dx.doi.org/10.1097/00005344-198500076-00004.

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9

Bose, D. "Cardiac excitation–contraction coupling: new developments." Canadian Journal of Physiology and Pharmacology 66, no. 9 (1988): 1217. http://dx.doi.org/10.1139/y88-200.

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Over 100 years have elapsed since Sidney Ringer made the serendipitous discovery that calcium played a crucial role in amphibian cardiac contraction. Since then we have learned that this ion is an obligatory requirement for cardiac muscle of all species, and that the regulation of intracellular calcium levels is considerably more complex in the mammalian heart than previously thought. Part of this complexity is due to the involved design requirements of mammalian physiological processes. Another element of complexity is introduced by the quantitative differences in the involvement of various r

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10

LEDERER, W. J., J. R. BERLIN, N. M. COHEN, R. W. HADLEY, D. M. BERS, and M. B. CANNELL. "Excitation-Contraction Coupling in Heart Cells." Annals of the New York Academy of Sciences 588, no. 1 Embryonic Ori (1990): 190–206. http://dx.doi.org/10.1111/j.1749-6632.1990.tb13210.x.

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11

Numa, S., T. Tanabe, H. Takeshima, et al. "Molecular Insights into Excitation-Contraction Coupling." Cold Spring Harbor Symposia on Quantitative Biology 55 (January 1, 1990): 1–7. http://dx.doi.org/10.1101/sqb.1990.055.01.003.

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12

Balke, C. William, and L. Goldman. "Excitation Contraction Coupling in Cardiac Muscle." Journal of General Physiology 121, no. 5 (2003): 349–52. http://dx.doi.org/10.1085/jgp.200308841.

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13

Lakatta, Edward G. "Excitation-Contraction Coupling in Heart Failure." Hospital Practice 26, no. 7 (1991): 85–98. http://dx.doi.org/10.1080/21548331.1991.11704209.

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14

Niggli, Ernst. "Basic mechanisms of excitation/contraction coupling." Journal of Molecular and Cellular Cardiology 40, no. 6 (2006): 923. http://dx.doi.org/10.1016/j.yjmcc.2006.03.023.

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15

Wallis, Helen L., Claire Sears, and Simon Bryant. "Regional Differences in Excitation-Contraction Coupling." Clinical Science 103, s47 (2002): 10P. http://dx.doi.org/10.1042/cs103010p.

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16

Hare, J. "Nitric oxide and excitation–contraction coupling." Journal of Molecular and Cellular Cardiology 35, no. 7 (2003): 719–29. http://dx.doi.org/10.1016/s0022-2828(03)00143-3.

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17

Ashcroft, Frances M. "Ca2+ channels and excitation-contraction coupling." Current Opinion in Cell Biology 3, no. 4 (1991): 671–75. http://dx.doi.org/10.1016/0955-0674(91)90040-6.

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18

Ikemoto, Noriaki, Michel Ronjat, and L�szr� G. M�sz�ros. "Kinetic analysis of excitation-contraction coupling." Journal of Bioenergetics and Biomembranes 21, no. 2 (1989): 247–66. http://dx.doi.org/10.1007/bf00812071.

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19

Melzer, W., and B. Dietze. "Malignant hyperthermia and excitation-contraction coupling." Acta Physiologica Scandinavica 171, no. 3 (2001): 367–78. http://dx.doi.org/10.1046/j.1365-201x.2001.00840.x.

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20

Caillé, J., M. Ildefonse, and O. Rougier. "Excitation-contraction coupling in skeletal muscle." Progress in Biophysics and Molecular Biology 46, no. 3 (1985): 185–239. http://dx.doi.org/10.1016/0079-6107(85)90009-4.

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21

Donaldson, Sue K., Esther M. Gallant, and Daniel A. Huetteman. "Skeletal muscle excitation-contraction coupling I." Pfl�gers Archiv European Journal of Physiology 414, no. 1 (1989): 15–23. http://dx.doi.org/10.1007/bf00585621.

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22

Gallant, Esther M., and Sue K. Donaldson. "Skeletal muscle excitation-contraction coupling II." Pfl�gers Archiv European Journal of Physiology 414, no. 1 (1989): 24–30. http://dx.doi.org/10.1007/bf00585622.

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23

Lamb, G. D. "DHP receptors and excitation-contraction coupling." Journal of Muscle Research and Cell Motility 13, no. 4 (1992): 394–405. http://dx.doi.org/10.1007/bf01738035.

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24

Maack, C., and B. O'Rourke. "Excitation-contraction coupling and mitochondrial energetics." Basic Research in Cardiology 102, no. 5 (2007): 369–92. http://dx.doi.org/10.1007/s00395-007-0666-z.

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25

Wray, Susan, Ursula Ravens, Alexei Verkhratsky, and David Eisner. "Two centuries of excitation–contraction coupling." Cell Calcium 35, no. 6 (2004): 485–89. http://dx.doi.org/10.1016/j.ceca.2004.01.004.

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26

Sanders, Kenton M., and Nelson G. Publicover. "Excitation-contraction coupling in gastric muscles." Digestive Diseases and Sciences 39, S12 (1994): 69S—72S. http://dx.doi.org/10.1007/bf02300375.

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27

Ebashi, Setsuro. "Excitation-Contraction Coupling and the Mechanism of Muscle Contraction." Annual Review of Physiology 53, no. 1 (1991): 1–17. http://dx.doi.org/10.1146/annurev.ph.53.030191.000245.

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28

Tao, Liang, Yu Huang, and Jean-Pierre Bourreau. "Control of the mode of excitation-contraction coupling by Ca2+ stores in bovine trachealis muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 4 (2000): L722—L732. http://dx.doi.org/10.1152/ajplung.2000.279.4.l722.

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Full muscarinic stimulation in bovine tracheal smooth muscle caused a sustained contraction and increase in intracellular Ca2+concentration ([Ca2+]i) that was largely resistant to inhibition by nifedipine. Depletion of internal Ca2+ stores with cyclopiazonic acid resulted in an increased efficacy of nifedipine to inhibit this contraction and the associated increase in [Ca2+]i. Thus internal Ca2+ store depletion promoted electromechanical coupling between full muscarinic stimulation and muscle contraction to the detriment of pharmacomechanical coupling. A similar change in coupling mode was ind

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29

Leong, Peng, and David H. MacLennan. "Complex interactions between skeletal muscle ryanodine receptor and dihydropyridine receptor proteins." Biochemistry and Cell Biology 76, no. 5 (1998): 681–94. http://dx.doi.org/10.1139/o98-079.

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Evidence for functional interactions between the Ca2+ release channel in the skeletal muscle sarcoplasmic reticulum (the ryanodine receptor) and the L-type Ca2+ channel in the sarcolemma (the dihydropyridine receptor), leading to excitation-contraction coupling, is reviewed and experimental systems used to identify candidate sites of interaction are outlined.Key words: sarcoplasmic reticulum, excitation-contraction coupling.

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30

Jungbluth, Heinz, Susan Treves, Francesco Zorzato, et al. "Congenital myopathies: disorders of excitation–contraction coupling and muscle contraction." Nature Reviews Neurology 14, no. 3 (2018): 151–67. http://dx.doi.org/10.1038/nrneurol.2017.191.

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31

Tohse, Noritsugu, Sumihiko Seki, Takeshi Kobayashi, Masaaki Tsutsuura, Masato Nagashima, and Yoichi Yamada. "Development of Excitation-Contraction Coupling in Cardiomyocytes." Japanese Journal of Physiology 54, no. 1 (2004): 1–6. http://dx.doi.org/10.2170/jjphysiol.54.1.

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32

Altamirano, Julio, and Donald M. Bers. "Voltage Dependence of Cardiac Excitation–Contraction Coupling." Circulation Research 101, no. 6 (2007): 590–97. http://dx.doi.org/10.1161/circresaha.107.152322.

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33

Lüllmann, Heinz, and Albrecht Ziegler. "Calcium, Cell Membrane, and Excitation-Contraction Coupling." Journal of Cardiovascular Pharmacology 10 (1987): S2—S8. http://dx.doi.org/10.1097/00005344-198710001-00002.

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34

Du, Wanglei, Timothy J. McMahon, Zhu-Shan Zhang, Jonathan A. Stiber, Gerhard Meissner, and Jerry P. Eu. "Excitation-Contraction Coupling in Airway Smooth Muscle." Journal of Biological Chemistry 281, no. 40 (2006): 30143–51. http://dx.doi.org/10.1074/jbc.m606541200.

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35

Fleischer, S., and M. Inui. "Biochemistry and Biophysics of Excitation-Contraction Coupling." Annual Review of Biophysics and Biophysical Chemistry 18, no. 1 (1989): 333–64. http://dx.doi.org/10.1146/annurev.bb.18.060189.002001.

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36

Goldhaber, Joshua I., and Mohammed S. Qayyum. "Oxygen Free Radicals and Excitation-Contraction Coupling." Antioxidants & Redox Signaling 2, no. 1 (2000): 55–64. http://dx.doi.org/10.1089/ars.2000.2.1-55.

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37

OGAWA, Y. "Ryanodine receptor isoforms in excitation-contraction coupling." Advances in Biophysics 36 (1999): 27–64. http://dx.doi.org/10.1016/s0065-227x(99)80004-5.

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38

Callewaert, G. "Excitation-contraction coupling in mammalian cardiac cells." Cardiovascular Research 26, no. 10 (1992): 923–32. http://dx.doi.org/10.1093/cvr/26.10.923.

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39

SHATTOCK, M. J. "Excitation-Contraction Coupling and Cardiac Contractile Force." Cardiovascular Research 26, no. 4 (1992): 430. http://dx.doi.org/10.1093/cvr/26.4.430.

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40

Aronsen, J. M., F. Swift, and O. M. Sejersted. "Cardiac sodium transport and excitation–contraction coupling." Journal of Molecular and Cellular Cardiology 61 (August 2013): 11–19. http://dx.doi.org/10.1016/j.yjmcc.2013.06.003.

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41

Bers, Donald M., and Yujie Zhu. "Excitation-Contraction Coupling and Cardiac Contractile Force." Journal of Cardiovascular Disease Research 1, no. 1 (2010): 45. http://dx.doi.org/10.1016/s0975-3583(10)11011-0.

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42

Sipido, K. "Triggering controversy in cardiac excitation–contraction coupling." Journal of Molecular and Cellular Cardiology 35, no. 2 (2003): 133–35. http://dx.doi.org/10.1016/s0022-2828(02)00311-5.

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43

Imai, Tomihiro. "122. Excitation–contraction coupling in the masseter." Clinical Neurophysiology 120, no. 5 (2009): e174-e175. http://dx.doi.org/10.1016/j.clinph.2009.02.128.

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44

Lee, K., H. Saito, and N. Matsuki. "Excitation-contraction coupling in suncus cardiac muscle." European Journal of Pharmacology 183, no. 4 (1990): 1224–25. http://dx.doi.org/10.1016/0014-2999(90)94322-o.

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45

Baum, V. C., and T. Klitzner. "EXCITATION-CONTRACTION COUPLING IN NEONATAL RABBIT MYOCARDIUM." Anesthesia & Analgesia 70, Supplement (1990): S17. http://dx.doi.org/10.1213/00000539-199002001-00017.

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46

Zucchi, Riccardo. "Effect of gallopamil on excitation-contraction coupling." General Pharmacology: The Vascular System 27, no. 5 (1996): 749–53. http://dx.doi.org/10.1016/0306-3623(95)02095-0.

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47

Brunton, Laurence L. "Excitation-contraction coupling and cardiac contractile force." Trends in Pharmacological Sciences 13 (January 1992): 297. http://dx.doi.org/10.1016/0165-6147(92)90091-j.

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48

Ullrich, Nina D., Mohammed Fanchaouy, Konstantin Gusev, Natalia Shirokova, and Ernst Niggli. "Hypersensitivity of excitation-contraction coupling in dystrophic cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 6 (2009): H1992—H2003. http://dx.doi.org/10.1152/ajpheart.00602.2009.

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Duchenne muscular dystrophy represents a severe inherited disease of striated muscle. It is caused by a mutation of the dystrophin gene and characterized by a progressive loss of skeletal muscle function. Most patients also develop a dystrophic cardiomyopathy, resulting in dilated hypertrophy and heart failure, but the cellular mechanisms leading to the deterioration of cardiac function remain elusive. In the present study, we tested whether defective excitation-contraction (E-C) coupling contributes to impaired cardiac performance. “E-C coupling gain” was determined in cardiomyocytes from con

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49

Bandi, Elena, Marko Jevšek, Tomaz Mars, et al. "Neural agrin controls maturation of the excitation-contraction coupling mechanism in human myotubes developing in vitro." American Journal of Physiology-Cell Physiology 294, no. 1 (2008): C66—C73. http://dx.doi.org/10.1152/ajpcell.00248.2007.

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The aim of this study was to elucidate the mechanisms responsible for the effects of innervation on the maturation of excitation-contraction coupling apparatus in human skeletal muscle. For this purpose, we compared the establishment of the excitation-contraction coupling mechanism in myotubes differentiated in four different experimental paradigms: 1) aneurally cultured, 2) cocultured with fetal rat spinal cord explants, 3) aneurally cultured in medium conditioned by cocultures, and 4) aneurally cultured in medium supplemented with purified recombinant chick neural agrin. Ca2+ imaging indicat

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50

Zhou, Yiqiu. "Excitation Contraction Coupling in Hypertrophy and Failing Heart Cells." E3S Web of Conferences 271 (2021): 03008. http://dx.doi.org/10.1051/e3sconf/202127103008.

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The contraction of the heart is dependent on a process named the excitation-contraction coupling (E-C coupling). In hypertrophy and failing heart models, the expression, phosphorylation and function of key calcium handling proteins involved in E-C coupling are altered. It’s important to figure out the relationship changes between calcium channel activity and calcium release from sarcoplasmic reticulum (SR). This review will therefore focus on novel components of E-C coupling dysfunction in hypertrophy and failing heart, such as L-type Ca2+ channel (LCC), ryanodine receptor type-2 channel (RyR2

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