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Dissertations / Theses on the topic 'Excitation-contraction coupling'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Xu, Liqun. "Ontogeny of myocardial excitation-contraction coupling." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ51512.pdf.

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2

Kane, Christopher. "Heterocellular regulation of cardiomyocyte excitation-contraction coupling." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/53120.

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Our understanding of cardiomyocyte electrophysiology and function has been built from experimentation on the single, isolated cardiomyocyte. As a result, a significant body of work has been accumulated describing the mechanisms underlying cardiomyocyte function in health, and how they are altered in disease. The heart however is a sophisticated syncytium of which cardiomyocytes comprise only one third of the cellular content, supported by a number of other cell types. It is the summation of these parts which underlies the effectiveness and adaptability of the heart as an organ, however our und

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3

Boonen, Henricus Cornelis Matjeu. "Excitation-contraction coupling in small arteries: role in hypertension." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1992. http://arno.unimaas.nl/show.cgi?fid=6510.

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4

Schulson, Meredith Nicole. "The structure of excitation-contraction coupling in atrial cardiomyocytes." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3981.

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Standard local control theory, which describes Ca²⁺ release during excitation-contraction coupling (ECC), assumes that all Ryanodine Receptor (RyR) complexes are equivalent. Recent data from our laboratory has called this assumption into question. Specifically, we have shown that RyR complexes in ventricular myocytes differ depending on their location within the cell. This, and other data, has led us to hypothesize that similar differences occur within the rat atrial cell. To test this hypothesis, we have triple-labeled enzymatically-isolated, fixed myocytes to examine the distribution and

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5

Tengah, Ampuan Haji Mohamad Asrin Ampuan Haji. "P2Y receptor-mediated excitation-contraction coupling in pulmonary arteries." Thesis, University of Strathclyde, 2010. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=14353.

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6

Wallis, Helen Loise. "Regional excitation-contraction coupling mechanisms in the mammalian heart." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398450.

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7

Miller, Stewart L. W. "A study of excitation contraction coupling in rabbit cardiomyocytes." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404445.

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8

Shabir, Saqib. "Rho-kinase and excitation-contraction coupling in ureter smooth muscle." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403218.

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9

Yoon, Samuel J. "Role of citrate toxicity on cardiac excitation-contraction coupling mechanisms." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0013/MQ29353.pdf.

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10

Collins, Helen Elizabeth. "Diurnal variation in excitation-contraction coupling in rat ventricular myocytes." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/29009.

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Diurnal variation has been reported in many cardiovascular haemodynamics parameters such as heart rate and blood pressure and the cardiac action potential. This variation may result from the diurnal variation in sympathetic activity or in cardiac gene expression. However, it is unknown whether these time-of-day dependent changes impact on excitation-contraction (EC) coupling. There is also a morning peak in the onset of ventricular arrhythmias and associated sudden cardiac death in man, which appear linked to the increase in sympathetic activity. Therefore, the aims of this investigation were

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11

bhattacharya, Sayak. "Regulation of Excitation-Contraction and Excitation-Transcription Coupling in Gastrointestinal Smooth Muscle by Caveolin-1." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2883.

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Caveolae are integral part of the smooth muscle membrane and caveolins, the defining proteins of caveolae, act as scaffolding proteins for several G protein-coupled receptor signaling molecules and regulate cellular signaling through direct and indirect interactions with signaling proteins. Caveolin-1 is the predominant isoform in the smooth muscle and drives the formation of caveolae. However, little is known about the role of caveolin-1 in the regulation of excitation-contraction and excitation-transcription coupling in gastrointestinal smooth muscle. In the present study we have characteriz

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12

Koivumäki, J. (Jussi). "Regulation of excitation-contraction coupling in cardiac myocytes:insights from mathematical modelling." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514293047.

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Abstract Background – The heart cell is a prime example of a system, in which numerous interconnected regulatory mechanisms affect the dynamic balance of cellular function. The function of the system emerges from the interactions of its components rather than from their individual properties. Thus, it is a challenging task to understand the causal relations within such a system, based on the analysis of experimental results. Facing this complexity, the systems biological approach has gained interest during recent years, since with using it we can make an effort to observe, quantitatively and s

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13

Lin, Tsai Jing Eric. "Distribution of excitation-contraction coupling proteins as a function of development." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/20563.

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Excitation-contraction (EC) coupling in the neonatal rabbit heart has been previously shown to be mediated predominately by reverse-mode activity of the sodium-calcium exchanger (NCX). Thus the regulation of NCX is a primary determinant of neonatal cardiac contractility. It is proposed that in neonate hearts, a restricted domain allows a sodium current (INa) to mediate a large elevation in subsarcolemmal sodium concentration which then drives calcium entry through reverse-mode NCX. Functional data suggest that calcium influx through NCX can also trigger calcium induced calcium release (CICR).

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14

Holmes, Janet. "Excitation-contraction coupling in muscles of the Norway lobster Nephrops norvegicus." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360168.

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15

Cros, Caroline. "From fish to mammals : new insights in cardiac excitation-contraction coupling." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/from-fish-to-mammals-new-insights-in-cardiac-excitationcontraction-coupling(a2fdffac-1ef7-4290-8169-3f50e42a33ff).html.

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Rationale and objectives: Mouse is currently the main model to study human diseases. However several aspects of murine biology limit its routine use in large-scale genetic. Recently, zebrafish (ZF) emerged as popular model for studying embryologically and genetically tractable diseases. Surprisingly, there is no information about the electrical activity of freshly isolated ventricular myocyte. The first part of the project addresses this point. Further, in fish, cardiac Ca cycling is almost exclusively driven by sarcolemmal Ca, such that excitation-contraction coupling occurs with little to no

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16

CHISCI, RICCARDO. "Akt-Pka interaction in the modulation of cardiac excitation - contraction coupling." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/7484.

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Derangement of sarcoplasmic reticulum (SR) function play a primary role in the pathogenesis of cardiac contractile deficit in heart failure (HF). The PI3K/AKT is a complex signalling pathway with a central role in the modulation of both cardiac function and structure; an imbalance in its components may contribute to contractile dysfunction and myocardial structural remodelling in HF. In particular, the cardiac contractility modulation, in which the PI3K/Akt pathway is involved, is mainly regulated by β-adrenergic signaling. The pleckstrin-homology (PH) domain is a highly conserved protein doma

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17

Freestone, Nicholas. "Effects of magnesium and calcium upon excitation-contraction coupling in the heart." Thesis, University of Central Lancashire, 1995. http://clok.uclan.ac.uk/20522/.

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Calcium (Ca2 ) availability to cardiac myofilaments is the primary factor determining the force of cardiac contraction. An intracellular organelle, the sarcoplasmic reticulum (SR), regulates the relaxation of the muscle as well as acting as a source of activating Ca2 during excitation-contraction coupling. Calcium metabolism in the heart undergoes developmental changes during early postnatal life and some of these changes may concern the activity of the SR. Using the technique of oxalate-supported Ca2 uptake into SR vesicles from rat hearts, the developmental changes in the activity of the SR

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18

Proven, Andrew Philip. "Endothelin-1 and Ca²⁺ mobilisation during excitation-contraction coupling in cardiac myocytes." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613903.

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19

Graham, Mark David. "The effects of anaesthetics on excitation-contraction coupling in intact ventricular myocytes." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424022.

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20

Dumitrescu, Cristian. "Excitation-contraction coupling and mechanical restitution in normal and failing rat hearts /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486397841223232.

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21

Morotti, Stefano <1984&gt. "Computational Modeling of Cardiac Excitation-Contraction Coupling in Physiological and Pathological Conditions." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5427/1/morotti_stefano_tesi.pdf.

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The cardiomyocyte is a complex biological system where many mechanisms interact non-linearly to regulate the coupling between electrical excitation and mechanical contraction. For this reason, the development of mathematical models is fundamental in the field of cardiac electrophysiology, where the use of computational tools has become complementary to the classical experimentation. My doctoral research has been focusing on the development of such models for investigating the regulation of ventricular excitation-contraction coupling at the single cell level. In particular, the following resear

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22

Morotti, Stefano <1984&gt. "Computational Modeling of Cardiac Excitation-Contraction Coupling in Physiological and Pathological Conditions." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5427/.

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The cardiomyocyte is a complex biological system where many mechanisms interact non-linearly to regulate the coupling between electrical excitation and mechanical contraction. For this reason, the development of mathematical models is fundamental in the field of cardiac electrophysiology, where the use of computational tools has become complementary to the classical experimentation. My doctoral research has been focusing on the development of such models for investigating the regulation of ventricular excitation-contraction coupling at the single cell level. In particular, the following resear

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23

Brenner, Tracy Lynn. "The physiology of crayfish intestinal striated muscle, histology, histochemistry, and excitation-contraction coupling." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ47992.pdf.

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24

Xiong, Wei. "Physiology and pharmacology of excitation-contraction coupling in normal and diseased cardiac cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ66662.pdf.

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25

Lee, Joon. "The effects of adult progenitor cell transplantation on recipient cardiomyocyte excitation-contraction coupling." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4250.

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Cell transplantation is a promising strategy for treating heart failure but the mechanisms effecting functional improvements remain unknown. The hypothesis that cell transplantation influences the contractile properties and excitation-contraction (EC) coupling of recipient cardiomyocytes by paracrine mechanisms was tested. Adult rats underwent myocardial infarction and subsequently developed chronic heart failure. They then received intra-myocardial injections of either skeletal myoblasts or bone marrow mononuclear cells which were harvested from transgenic rats constitutively expressing green

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26

Griffiths, Huw. "Evaluation of the voltage sensitive release mechanism of excitation contraction coupling in cardiac muscle." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399578.

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27

Rakovic, Stevan. "Possible influence of cADP-ribose on excitation-contraction coupling in isolated cardiac ventricular myocytes." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318856.

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28

Giembycz, M. A. "Some biochemical and pharmacological studies on excitation-contraction coupling and uncoupling in mammalian lung." Thesis, University of Strathclyde, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381500.

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29

Bent, Sarah Louise. "The role of calmodulin in decoding the calcium signal in muscle excitation-contraction coupling." Thesis, University of Manchester, 2011. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549335.

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30

Semont, Audrey. "Implication des ROS mitochondriaux dans le couplage excitation contraction cardiaque." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0426.

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L’activation électrique des cardiomyocytes, via le courant de dépolarisation qu’elle induit, est primordiale dans la contraction cardiaque qui requiert l’adéquation de la production d'énergie par les mitochondries et des besoins énergétiques de l’appareil contractile. Les espèces radicalaires de l'oxygène (ROS) ont été récemment impliquées dans la régulation de nombreux acteurs du couplage excitation-contraction cardiaque. L’objectif de ce travail est d’explorer l'implication des ROS d'origine mitochondriale dans la régulation du couplage excitation-contraction au niveau du cardiomyocyte, en c

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31

Xue, Wei. "Expression and role of PKC in control of excitation-contraction coupling in ureter smooth muscle." Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501562.

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The aim of this work was to investigate possible role of PKC in control of excitation-contraction coupling in phasic guinea pig and rat ureter smooth muscle. Immunohistochemistry and western blotting were used to identify the expression of four PKC isoforms α, β, δ and ε in ureter smooth muscle of both species. Photometric system combined with force measurement and electrical activity as well as confocal imaging of isolated ureteric myocites have been used in the functional studies. The effects of PKC activator PDBu and PKC inhibitor Ro320432 on force and Ca²⁺ induced by different modes of sti

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32

Mackenzie, Lauren. "Spatiotemporal properties of calcium signalling during excitation-contraction coupling in isolated rat atrial cardiac myocytes." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621399.

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33

Lau, Chun-hung Barry, and 劉俊雄. "Excitation contraction coupling of ventricular myocyte in septicshock: role of a change in calcium cyclingsystem." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558320.

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34

Wallace, Patrick. "Excitation/contraction coupling in mouse anococcygeus smooth muscle : a role for store-operated calcium entry." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424303.

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35

Patel, Kiranbhai C. R. "Excitation - contraction coupling in cardiac muscle : the role of membrane potential and transmembrane Ca entry." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364936.

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36

Pabbathi, Vijay Kumar. "Excitation-contraction coupling in mammalian heart muscle : control by membrane potential and calcium ion entry?" Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393923.

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37

Corona, Benjamin T. "Junctophilin Damage Contributes to Early Force Deficits and Excitation-Contraction Coupling Failure after Performing Eccentric Contractions." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/kin_health_diss/4.

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Junctophilins (JP1 & JP2) are expressed in skeletal muscle and are the primary proteins involved in transverse (T)-tubule and sarcoplasmic reticulum (SR) membrane apposition. During the performance of eccentric contractions, the apposition of T-tubule and SR membranes may be disrupted, resulting in excitation-contraction (EC) coupling failure and thus reduced force-producing capacity. In this study, we made three primary observations: 1) Through the first three days after the performance of 50 eccentric contractions in vivo by the left hindlimb anterior crural muscles of female mice, both JP1

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38

Korhonen, T. (Topi). "Mathematical modeling of the regulation, development and genetically engineered experimental models of cardiac excitation-contraction coupling." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514290756.

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Abstract Excitation-contraction coupling (ECC) is a process linking the electrical excitation of the muscle cell (myocyte) membrane to the contraction of the cell. In this study the possibilities of mathematical modeling were studied in current ECC research. Mathematical modeling was employed in two distinct ECC research areas, the enzymatic regulation of ECC and ECC during cardiac myocyte development. Despite the distinction, both of these are extremely complex biological systems characterized by diverse and partly contradictory reported experimental results, with a large part based on genet

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39

Cartledge, James. "The effects of cardiac fibroblasts on cardiac myocyte structure and excitation-contraction coupling through paracrine mediators." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14201.

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Cardiac fibroblasts are the most numerous cells within the heart. Their traditional roles are the maintenance of the extracellular matrix to support the structure and contraction of the heart, and their activation and production of increased extracellular matrix in disease. Over the past 15 years, evidence has grown that shows fibroblasts are capable of modulating myocyte function. This is achieved through paracrine mediators, the release of biologically active soluble substances into the local environment, and through direct cell contact, involving gap junctions and mechanical connections. Fi

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40

Amoako, Daniel Kwasi. "Cyclopiazonic acid changes the mode of excitation-contraction coupling in acetylcholine-stimulated bovine tracheal smooth muscle /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1865017X.

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41

Meschin, Pierre. "Régulations monoaminergiques AMPc-dépendantes du coeur sain et pathologique." Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON1T010.

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La fonction cardiaque est finement régulée par des hormones de type monoamines qui constituent des régulateurs cruciaux de l’activité cardiaque (chronotropie et inotropie). Ces hormones dérivées d’acides aminés aromatiques comprenant les catécholamines et la sérotonine maintiennent l’activité du myocarde dans un cadre physiologique tout en lui permettant de s’adapter aux contraintes environnementales. Les récepteurs cellulaires des monoamines sont couplés à des voies de signalisation qui impliquent un nucléotide cyclique, l’AMPc, et modulent la contractilité des cardiomyocytes par l’intermédia

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42

Lau, Chun-hung Barry. "Excitation contraction coupling of ventricular myocyte in septic shock : role of a change in calcium cycling system /." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39558320.

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43

Pan, Yuan [Verfasser]. "Functional consequences of two critical point mutations in the skeletal muscle excitation-contraction coupling complex / Yuan Pan." Ulm : Universität Ulm, 2020. http://d-nb.info/1204132534/34.

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44

Roberge, Stéphanie. "Caractérisation des voies de mort cellulaire lors du remodelage cardiaque dans les cardiopathies d'origine ischémique." Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON1T027.

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L'ischémie se caractérise par l'obstruction d'une artère coronaire qui prive le tissu d'un apport en oxygène et nutriments. Bien que nécessaire, la reperfusion, c'est-à-dire la réouverture de l'artère, s'accompagne de lésions tissulaires, appelées lésions de reperfusion. Au cours de l'I/R, le TNF-α, cytokine pro-inflammatoire, augmente. Sa liaison sur son récepteur TNFR1 induit le recrutement des protéines FADD et procaspase-8 formant le complexe DISC qui permet l'activation de la caspase-8. La caspase-8 clive une protéine pro-apoptotique, Bid, qui induit une perméabilisation de la membrane mi

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45

Ferrantini, Cecilia, Raffaele Coppini, Josè Manuel Pioner, et al. "Pathogenesis of Hypertrophic Cardiomyopathy is Mutation Rather Than Disease Specific: A Comparison of the Cardiac Troponin T E163R and R92Q Mouse Models." WILEY, 2017. http://hdl.handle.net/10150/625498.

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Background-In cardiomyocytes from patients with hypertrophic cardiomyopathy, mechanical dysfunction and arrhythmogenicity are caused by mutation-driven changes in myofilament function combined with excitation-contraction (E-C) coupling abnormalities related to adverse remodeling. Whether myofilament or E-C coupling alterations are more relevant in disease development is unknown. Here, we aim to investigate whether the relative roles of myofilament dysfunction and E-C coupling remodeling in determining the hypertrophic cardiomyopathy phenotype are mutation specific. Methods and Results-Two hype

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46

Hobai, Ion Alexandru. "Excitation - contraction coupling in heart muscle : the roles of L-type Ca channels, Na/Ca exchange and membrane potential." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263826.

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47

Crumbie, Hayley Elizabeth. "Beta-adrenergic receptor signalling and excitation-contraction coupling in the heart : impact of circadian rhythms and beta-3 receptors." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37500.

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A time-of-day variation in myocardial contraction and its response to sympathetic stimulation of β-adrenoceptors (b-ADR) exists, which is reflected by time-of-day variations in intracellular calcium [Ca2+]i regulation and electrical activity. There are three isoforms of β-ADR (β1/β2/β3) and the functional outcome of each receptor differs. β1/β2-ADRs result in positive inotropism, whereas β3-ADR induces a negative inotropic effect, associated with nitric oxide (NO) signalling. The aims of this thesis were to determine the role of the β3-ADR in the time-of-day variation in the response to sympat

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48

Eley, Douglas W. "Mechanisms involved in the disruption and restoration of excitation-contraction coupling in the rat myocardium by hypochlorous acid and dithiothreitol." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7601.

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In the present studies, the addition of HOCl to the bathing medium for isometrically contracting papillary rat papillary muscles induced the development of contracture. This was characterized by a decline in developed tension (DT) in combination with a rise in resting tension (RT), a prolongation in relaxation kinetics, and a sensitivity of the muscles to stimulation voltage. This response to HOCl was potentiated by preincubation with low extracellular Ca$\sp{2+}$ or the Ca$\sp{2+}$ channel antagonist nifedipine. Conversely, the response was attenuated by preincubation with high extracellular

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49

Filipova, Dilyana [Verfasser], Niels [Gutachter] Gehring, and Stefan [Gutachter] Herzig. "From excitation-contraction coupling to gene expression: Roles of RYR1 and Cav1.1 in myogenesis / Dilyana Filipova ; Gutachter: Niels Gehring, Stefan Herzig." Köln : Universitäts- und Stadtbibliothek Köln, 2018. http://d-nb.info/1165772779/34.

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50

Fantozzi, Ivana. "Study of the regulation of excitation-contraction coupling in vascular smooth muscle : the cellular and the molecular mechanisms of pulmonary hypertension." Nice, 2004. http://www.theses.fr/2004NICE4010.

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L'hypertrophie vasculaire médiane pulmonaire dans l'hypertension pulmonaire primaire (PPH) est principalement liée à une augmentation de la prolifération et à une diminution de l'apoptose dans les cellules du muscle lisse de l'artère pulmonaire humaine (PASMCs). Le premier objectif de cette étude était d'élucider la pathogenèse PPH. Dans un premier temps, j'ai examiné les effets apoptotiques des protéines morphogénétiques osseuses (BMPs) sur les cellules PASMCs humaines normales et analyse si les effets induits par les BMPs sont altérés dans les cellules PASMCs de patients PPH. Le traitement d

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