Log in

Relevant bibliographies by topics / Calcium in muscle contraction

Contents

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers
Reports

Academic literature on the topic 'Calcium in muscle contraction'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Calcium in muscle contraction.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Calcium in muscle contraction"

1

Yu, Ming-Fu, Isabelle Gorenne, Xiaoling Su, Robert S. Moreland, and Michael I. Kotlikoff. "Sodium hydrosulfite contractions of smooth muscle are calcium and myosin phosphorylation independent." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 5 (November 1, 1998): L976—L982. http://dx.doi.org/10.1152/ajplung.1998.275.5.l976.

Full text

Abstract:

In an effort to further understand the processes underlying hypoxic pulmonary vasoconstriction, we examined the mechanism by which sodium hydrosulfite (Na2S2O4), a potent reducing agent and oxygen scavenger, induces smooth muscle contraction. In rat pulmonary arterial strips, sodium hydrosulfite (10 mM) induced contractions that were 65.9 ± 12.8% of the response to 60 mM KCl ( n = 9 segments). Contractions were not inhibited by nisoldipine (5 μM) or by repeated stimulation with caffeine (10 mM), carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (10 μM), or cyclopiazonic acid (10 μM), all of which eliminated responses to contractile agonists. Maximum force generation after exposure to sodium hydrosulfite was 0.123 ± 0.013 mN in the presence of 1.8 mM calcium and 0.127 ± 0.015 mN in the absence of calcium. Sodium hydrosulfite contractions in pulmonary arterial segments were not due to the generation of H2O2and occurred in the presence of chelerythrine (10 μM), which blocked phorbol ester contractions, and solution hyperoxygenation. Similar contractile responses were obtained in rat aortic and tracheal smooth muscles. Finally, contractions occurred in the complete absence of an increase in myosin light chain phosphorylation. Therefore sodium hydrosulfite-induced smooth muscle contraction is not specific to pulmonary arterial smooth muscle, is independent of calcium and myosin light chain phosphorylation, and is not mediated by either hypoxia or protein kinase C.

APA, Harvard, Vancouver, ISO, and other styles

2

Gunst, S. J., and J. M. Pisoni. "Effects of extracellular calcium on canine tracheal smooth muscle." Journal of Applied Physiology 61, no. 2 (August 1, 1986): 706–11. http://dx.doi.org/10.1152/jappl.1986.61.2.706.

Full text

Abstract:

Strips of canine tracheal smooth muscle were studied in vitro to determine the effects of changes in the extracellular calcium (Cao) concentration on tonic contractions induced by acetylcholine and 5-hydroxytryptamine. Strips were contracted with graded concentrations of the above agents in 2.4 mM Ca, after which CaCl2 was administered to achieve final concentrations of 5.0, 10.0, and 20.0 mM. Increases in Cao to 5 mM or above caused significant relaxation of muscles contracted with 5-hydroxytryptamine but did not significantly relax muscles contracted with acetylcholine. Increases in Cao also caused significant relaxation of muscles contracted with low concentrations of K+ (20 or 30 mM). However, in 60 or 120 mM K+, increases in Cao resulted predominantly in muscle contraction. Inhibition of the Na+-K+-ATPase by ouabain (10(-5) M) or K+ depletion reversed the effects of Cao from relaxation to contraction in tissues contracted with 5-hydroxytryptamine. Increases in Cao also caused contraction rather than relaxation in the presence of verapamil (10(-6) M). We conclude that calcium has both excitatory and inhibitory effects on the contractile responses of canine tracheal smooth muscle. The inhibitory effects of Ca2+ appear to be linked to the activity of the membrane Na+-K+-ATPase.

APA, Harvard, Vancouver, ISO, and other styles

3

Pelaez, Nancy J., Tracey R. Braun, Richard J. Paul, Richard A. Meiss, and C. Subah Packer. "H2O2 mediates Ca2+- and MLC20phosphorylation-independent contraction in intact and permeabilized vascular muscle." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 3 (September 1, 2000): H1185—H1193. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h1185.

Full text

Abstract:

One purpose of the current study was to establish whether vasoconstriction occurs in all vessel types in response to H2O2. Isometric force was measured in pulmonary venous and arterial rings, and isobaric contractions were measured in mesenteric arteries and veins in response to H2O2. A second purpose was to determine whether H2O2-induced contraction is calcium independent. The addition of H2O2 to calcium-depleted (using the Ca2+ ionophore ionomycin in zero calcium EGTA buffer) muscle caused contraction. Furthermore, permeabilized muscle contracted in response to H2O2 even in zero Ca2+. The final purpose was to determine whether the 20-kDa regulatory myosin light chain (MLC20) phosphorylation plays a role in H2O2-induced contraction. Pulmonary arterial strips were freeze-clamped at various time points during H2O2-induced contractions, and the relative amounts of phosphorylated MLC20 were measured. H2O2 caused dose-dependent contractions that were independent of MLC20 phosphorylation. ML-9, a myosin light chain kinase inhibitor, had no effect on the H2O2 contractile response. In conclusion, H2O2 induces Ca2+- and MLC20 phosphorylation-independent contraction in pulmonary and systemic arterial and venous smooth muscle.

APA, Harvard, Vancouver, ISO, and other styles

4

Parkman, Henry P., Arlene N. James, and James P. Ryan. "The contractile action of platelet-activating factor on gallbladder smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 1 (July 1, 2000): G67—G72. http://dx.doi.org/10.1152/ajpgi.2000.279.1.g67.

Full text

Abstract:

Platelet-activating factor (PAF) may be a mediator of some sequelae of cholecystitis, a disorder with gallbladder motor dysfunction. The aims of this study were to determine the effect and mechanism of PAF on gallbladder muscle. Exogenous administration of PAF-16 or PAF-18 caused dose-dependent contractions of gallbladder muscle strips in vitro with threshold doses of 1 ng/ml and 10 ng/ml, respectively. The PAF-induced contractions were not significantly reduced by TTX, atropine, or hexamethonium but were significantly inhibited with the PAF receptor antagonists ginkolide B and CV-3988. The PAF-induced contraction was reduced by indomethacin. Preventing influx of extracellular calcium with a calcium-free solution nearly abolished the PAF contractile response. Nifedipine inhibited the PAF contractile response, whereas ryanodine had no effect. Pertussis toxin reduced the PAF contractile response. In conclusion, PAF causes gallbladder contraction through specific PAF receptors on gallbladder muscle. These PAF receptors appear to be linked to a prostaglandin-mediated mechanism and to pertussis toxin-sensitive G proteins. The contractile response is largely mediated through the utilization of extracellular calcium influx through voltage-dependent calcium channels.

APA, Harvard, Vancouver, ISO, and other styles

5

Ng, Rainer, Joseph M. Metzger, Dennis R. Claflin, and John A. Faulkner. "Poloxamer 188 reduces the contraction-induced force decline in lumbrical muscles from mdx mice." American Journal of Physiology-Cell Physiology 295, no. 1 (July 2008): C146—C150. http://dx.doi.org/10.1152/ajpcell.00017.2008.

Full text

Abstract:

Duchenne Muscular Dystrophy is a genetic disease caused by the lack of the protein dystrophin. Dystrophic muscles are highly susceptible to contraction-induced injury, and following contractile activity, have disrupted plasma membranes that allow leakage of calcium ions into muscle fibers. Because of the direct relationship between increased intracellular calcium concentration and muscle dysfunction, therapeutic outcomes may be achieved through the identification and restriction of calcium influx pathways. Our purpose was to determine the contribution of sarcolemmal lesions to the force deficits caused by contraction-induced injury in dystrophic skeletal muscles. Using isolated lumbrical muscles from dystrophic ( mdx) mice, we demonstrate for the first time that poloxamer 188 (P188), a membrane-sealing poloxamer, is effective in reducing the force deficit in a whole mdx skeletal muscle. A reduction in force deficit was also observed in mdx muscles that were exposed to a calcium-free environment. These results, coupled with previous observations of calcium entry into mdx muscle fibers during a similar contraction protocol, support the interpretation that extracellular calcium enters through sarcolemmal lesions and contributes to the force deficit observed in mdx muscles. The results provide a basis for potential therapeutic strategies directed at membrane stabilization of dystrophin-deficient skeletal muscle fibers.

APA, Harvard, Vancouver, ISO, and other styles

6

SZENT-GYORGYI, A. G. "Muscle Contraction: Calcium in Muscle Activation." Science 238, no. 4824 (October 9, 1987): 223. http://dx.doi.org/10.1126/science.238.4824.223.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

McWilliam, T. M., A. Liepins, and A. J. Rankin. "Deuterium oxide reduces agonist and depoiarization-induced contraction of rat aortic rings." Canadian Journal of Physiology and Pharmacology 68, no. 12 (December 1, 1990): 1542–47. http://dx.doi.org/10.1139/y90-234.

Full text

Abstract:

The influence of deuterium oxide (D2O) on calcium-dependent vascular smooth muscle contraction was investigated. The effect of D2O on receptor-operated calcium channels was investigated with phenylephrine-induced contraction in the rat aortic ring preparation. D2O depressed the contraction response in a dose-dependent manner with 50% inhibition of maximum contraction observed with 60% D2O. The effect of 60% D2O on phenylephrine-induced contraction was reversible and not dependent on an intact endothelium. Sixty percent D2O also reduced potassium chloride induced contractions by 50%, indicating an effect on voltage-operated calcium channels. Studies with Bay K 8644, and L-type calcium channel activator, confirm an effect on utilization of extracellular calcium sources and on the voltage-operated calcium channel. Sixty percent D2O also depressed a calcium contraction dose–response curve by approximately 25%. Likewise, a change in the pD2′ for nifedipine in the presence of D2O may indicate an effect on the nifedipine binding site and (or) the voltage-dependent calcium channel. Further studies were performed to determine whether the D2O effects were nonspecific or selective effects on the receptor- and voltage-operated calcium channels. Sucrose-induced contaction in the presence of 60% D2O was found to be inhibited by approximately 50%. D2O similarly affected isoprenaline relaxation, which would suggest a nonspecific D2O effect on the vascular smooth muscle contractile process.Key words: deuterium oxide, vascular smooth muscle, calcium channels, rat aorta.

APA, Harvard, Vancouver, ISO, and other styles

8

Smith, Ian C., Rene Vandenboom, and A. Russell Tupling. "Caffeine attenuates contraction-induced diminutions of the intracellular calcium transient in mouse lumbrical muscle ex vivo." Canadian Journal of Physiology and Pharmacology 97, no. 5 (May 2019): 429–35. http://dx.doi.org/10.1139/cjpp-2018-0658.

Full text

Abstract:

The amount of calcium released from the sarcoplasmic reticulum in skeletal muscle rapidly declines during repeated twitch contractions. In this study, we test the hypothesis that caffeine can mitigate these contraction-induced declines in calcium release. Lumbrical muscles were isolated from male C57BL/6 mice and loaded with the calcium-sensitive indicator, AM-furaptra. Muscles were then stimulated at 8 Hz for 2.0 s in the presence or absence of 0.5 mM caffeine, at either 30 °C or 37 °C. The amplitude and area of the furaptra-based intracellular calcium transients and force produced during twitch contractions were calculated. For each of these measures, the values for twitch 16 relative to twitch 1 were higher in the presence of caffeine than in the absence of caffeine at both temperatures. We conclude that caffeine can attenuate contraction-induced diminutions of calcium release during repeated twitch contractions, thereby contributing to the inotropic effects of caffeine.

APA, Harvard, Vancouver, ISO, and other styles

9

Jiang, He, and Newman L. Stephens. "Calcium and smooth muscle contraction." Molecular and Cellular Biochemistry 135, no. 1 (1994): 1–9. http://dx.doi.org/10.1007/bf00925956.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Su, Xiaoling, Elaine M. Smolock, Kristi N. Marcel, and Robert S. Moreland. "Phosphatidylinositol 3-kinase modulates vascular smooth muscle contraction by calcium and myosin light chain phosphorylation-independent and -dependent pathways." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 2 (February 2004): H657—H666. http://dx.doi.org/10.1152/ajpheart.00497.2003.

Full text

Abstract:

Regulation of smooth muscle contraction involves a number of signaling mechanisms that include both kinase and phosphatase reactions. The goal of the present study was to determine the role of one such kinase, phosphatidylinositol (PI)3-kinase, in vascular smooth muscle excitation-contraction coupling. Using intact medial strips of the swine carotid artery, we found that inhibition of PI3-kinase by LY-294002 resulted in a concentration-dependent decrease in the contractile response to both agonist stimulation and membrane depolarization-dependent contractions and a decrease in Ca2+-dependent myosin light chain (MLC) phosphorylation, the primary step in the initiation of smooth muscle contraction. Inhibition of PI3-kinase also depressed phorbol dibutyrate-induced contractions, which are not dependent on either Ca2+ or MLC phosphorylation but are dependent on protein kinase C. To determine the Ca2+-dependent site of action of PI3-kinase, we determined the effect of several inhibitors of calcium metabolism on LY-294002-dependent inhibition of contraction. These inhibitors included nifedipine, SK&F-96365, and caffeine. Only SK&F-96365 blocked the LY-294002-dependent inhibition of contraction. Interestingly, all compounds blocked the LY-294002-dependent inhibition of MLC phosphorylation. Our results suggest that activation of PI3-kinase is involved in a Ca2+- and MLC phosphorylation-independent pathway for contraction likely to involve protein kinase C. In addition, our results also suggest that activation of PI3-kinase is involved in Ca2+-dependent signaling at the level of receptor-operated calcium channels.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Calcium in muscle contraction"

1

Masters, Jonathan Grenville. "Sources of calcium involved in detrusor smooth muscle contraction." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312030.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Aydin, Jan. "Skeletal muscle calcium homeostasis during fatigue : modulation by kinases and mitochondria /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-247-7/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

McCloskey, Diana Teresa. "Adrenergic regulation of cardiac muscle contraction and relaxation." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324975.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Stefanova, Helena Ivanova. "Calcium and phosphate transport in sarcoplasmic reticulum." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303376.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Gomez, Maria. "Calcium channel activity and force regulation in smooth muscle effects of polyamines and growth stimulation /." Lund : Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/68945015.html.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Smyrnias, Ioannis. "Modulation of contractility and calcium signalling in cardiac myocytes." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609227.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Sher, Anna. "Modelling local calcium dynamics and the sodium/calcium exchanger in ventricular myocytes." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670114.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Lynn, Stephen. "The ryanodine receptor channel complex in human smooth muscle cells." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285789.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Mulligan, Ian Patrick. "Mechanical studies on skinned muscle fibres using caged ATP and caged calcium." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258249.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Norman, Catalina. "Influence of the thin filament calcium activation on muscle force production and rate of contraction in cardiac muscle." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1178751966.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Calcium in muscle contraction"

1

Rüegg, Johann Caspar. Calcium in Muscle Contraction. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Rüegg, Johann Caspar. Calcium in muscle contraction: Cellular andmolecular physiology. 2nd ed. Berlin: Springer-Verlag, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Rüegg, Johann Caspar. Calcium in Muscle Contraction: Cellular and Molecular Physiology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Rüegg, Johann Caspar. Calcium in muscle contraction: Cellular and molecular physiology. 2nd ed. Berlin: Springer-Verlag, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

5

S, Moreland Robert, and Graduate Hospital (Philadelphia, Pa.), eds. Regulation of smooth muscle contraction. New York: Plenum Press, 1991.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

6

Calcium in muscle activation: A comparative approach. 2nd ed. Berlin: Springer-Verlag, 1988.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

7

Calcium in muscle activation: A comparative approach. Berlin: Springer-Verlag, 1986.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

8

Rüegg, Johann Caspar. Calcium in muscle activation: A comparative approach. Berlin: Springer-Verlag, 1986.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

9

Bianchi, C. Paul, George B. Frank, and H. E. D. J. ter Keurs. Excitation-contraction coupling in skeletal, cardiac, and smooth muscle. New York: Springer, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

10

Yamada Conference on Calcium as Cell Signal (1994 Tokyo, Japan). Calcium as cell signal: Proceedings of the Yamada Conference XXXIX on Calcium as Cell Signal, April 26-28, 1994, Tokyo, Japan. Tokyo: Igaku-Shoin, 1996.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "Calcium in muscle contraction"

1

Rüegg, Johann Caspar. "Vertebrate Smooth Muscle." In Calcium in Muscle Contraction, 201–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Rüegg, Johann Caspar. "Muscle Excitation and Contraction." In Calcium in Muscle Contraction, 3–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Endo, Makoto. "Muscle Contraction and Calcium Ion." In Muscle Relaxants, 48. Tokyo: Springer Japan, 1995. http://dx.doi.org/10.1007/978-4-431-66896-1_7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Rüegg, Johann Caspar. "Principles of Calcium Signalling in Muscle." In Calcium in Muscle Contraction, 239–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_10.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Rüegg, Johann Caspar. "Introduction." In Calcium in Muscle Contraction, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Rüegg, Johann Caspar. "Molecular Level Approaches to Excitation-Contraction Coupling in Heart and Skeletal Muscle." In Calcium in Muscle Contraction, 251–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_11.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Rüegg, Johann Caspar. "The Sarcoplasmic Reticulum: Storage and Release of Calcium." In Calcium in Muscle Contraction, 29–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Rüegg, Johann Caspar. "The Dependence of Muscle Contraction and Relaxation on the Intracellular Concentration of Free Calcium Ions." In Calcium in Muscle Contraction, 59–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Rüegg, Johann Caspar. "Calcium Binding and Regulatory Proteins." In Calcium in Muscle Contraction, 83–114. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Rüegg, Johann Caspar. "Diversity of Fast and Slow Striated Muscle." In Calcium in Muscle Contraction, 115–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77560-4_6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Calcium in muscle contraction"

1

Valdez, Chris, Michael B. Jirjis, Caleb C. Roth, Ronald A. Barnes, and Bennett L. Ibey. "Nanosecond electric pulses modulate skeletal muscle calcium dynamics and contraction." In SPIE BiOS, edited by Thomas P. Ryan. SPIE, 2017. http://dx.doi.org/10.1117/12.2253693.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Gupta, Suranjana, and Rohit Manchanda. "A Computational Study on the Effect of Intracellular Calcium Concentration and ATP on Detrusor Smooth Muscle Contraction." In 2019 9th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2019. http://dx.doi.org/10.1109/ner.2019.8716922.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Li, Yali, and N. C. Goulbourne. "Electro-Chemo-Mechanical Modeling of the Artery Myogenic Transient and Steady-State Response." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39237.

Full text

Abstract:

Active contraction of smooth muscle results in the myogenic response and vasomotion of arteries, which adjusts the blood flow and nutrient supply of the organism. It is a multiphysic process coupled electrical and chemical kinetics with mechanical behavior of the smooth muscle. This paper presents a new constitutive model for the media layer of the artery wall to describe the myogenic response of artery wall for different transmural pressures. The model includes two major components: electrobiochemical, and chemomechanical parts. The electrochemical model is a lumped Hodgkin-Huxley-type cell membrane model for the nanoscopic ionic currents: calcium, sodium, and potassium. The calculated calcium concentration serves as input for the chemomechanical portion of the model; its molecular binding and the reactions with other enzyme cause the relative sliding of thin and thick filaments of the contractile unit. In the chemomechanical model, a new nonlinear viscoelastic model is proposed using a continuum mechanics approach to describe the time varying behavior of the smooth muscle. Specifically, this model captures the filament overlap effect, active stress evolution, initial velocity, and elastic recoil in the media layer. The artery wall is considered as a thin-walled cylindrical tube. Using the proposed constitutive model and the thin-walled equilibrium equation, the myogenic response is calculated for different transmural pressures. The integrated model is able to capture the pressure-diameter transient and steady-state relationship.

APA, Harvard, Vancouver, ISO, and other styles

4

Sharma, N., P. M. Patre, C. M. Gregory, and W. E. Dixon. "Nonlinear Control of NMES: Incorporating Fatigue and Calcium Dynamics." In ASME 2009 Dynamic Systems and Control Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/dscc2009-2642.

Full text

Abstract:

Neuromuscular electrical stimulation (NMES) is a promising technique that has the potential to restore functional tasks in persons with movement disorders. Clinical and commercial NMES products exist for this purpose, but a pervasive problem with current technology is that overstimulation of the muscle (among other factors) leads to muscle fatigue. The objective of the current effort is to develop a NMES controller that incorporates the effects of muscle fatigue through an uncertain function of the calcium dynamics. A neural network-based estimate of the fatigue model mismatch is incorporated in a nonlinear controller through a backstepping based method to control the human quadriceps femoris muscle undergoing non-isometric contractions. The developed controller is proven to yield uniformly ultimately bounded stability for an uncertain nonlinear muscle model in the presence of bounded nonlinear disturbances (e.g., spasticity, delays, changing load dynamics).

APA, Harvard, Vancouver, ISO, and other styles

5

Nagatomi, Jiro, Michael B. Chancellor, and Michael S. Sacks. "Active Biaxial Mechanical Properties of Bladder Wall Tissue." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43146.

Full text

Abstract:

The urinary bladder is a smooth muscle organ whose main functions are to store and to void urine. Since the most important aspect of the storage function of the bladder is to maintain low intravesical pressure in order to protect the upper urinary tract from backflow of urine, the compliance of the bladder wall is one of the key functional paramters to assess the health of this organ. Previously, our laboratory reported, for the first time, the biaxial mechanical properties of bladder wall tissue in the inactive state (in the absence of calcium in the testing bath solution and thus smooth muscle contraction was abolished) (Gloeckner et al. 2002). The bladder in vivo, however, normaly exhibits passive smooth muscle tone during filling and active contraction during voiding. Therefore, in order to completely characterize the bladder tissue mechanical behaviors, it is necessary to examine the load-deformation relationship of the bladder under the passive and active states. In the present study, a novel experimental model was designed to allow collection of biaxial stress-strain data from urinary bladder wall tissue under passive, active and inactive states.

APA, Harvard, Vancouver, ISO, and other styles

6

Sheikh, Abdul Q., Jennifer R. Hurley, and Daria A. Narmoneva. "Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial Cells." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53797.

Full text

Abstract:

Diabetic cardiomyopathy (DCM) is a serious diabetes-associated complication that results in myocardial dysfunction independent of other etiological factors [1]. Pathological alterations to the myocardium associated with DCM include circulatory defects, impaired heart muscle contraction, and abnormal calcium (Ca2+) homeostasis in cardiac cells[2]. In myocardium, endothelial cells play an essential role in maintaining intracellular Ca2+ hemostasis in response to stimuli and regulating cardiac function [3]. External stimulus may cause abrupt changes in Ca2+ balance, including Ca2+ release from sarco-endoplasmic reticulum (ER) [4]. Subsequent return of the Ca2+ level to basal levels occurs due to Ca2+ decay mechanism, which is mainly regulated by sarco-endoplasmic reticulum Ca2+ ATPase pumps (SERCA) present at ER membrane which are responsible for Ca2+ sequestration [5]. Studies have shown that the mechanisms by which Ca2+ homeostasis alters cardiac function in diabetic cardiomyocytes include reduced activity of the SERCA pumps [6]. However, no information is available regarding the effects of diabetes on Ca2+ hemostasis and the underlying Ca2+ sequestration mechanism in diabetic cardiac endothelial cells[7]. This study tested the hypothesis that diabetic endothelial cells will exhibit disruptions in Ca2+ decay kinetics via alterations in the sequestration mechanism.

APA, Harvard, Vancouver, ISO, and other styles

7

Jafarnejad, Mohammad, Walter E. Cromer, Roland R. Kaunas, David C. Zawieja, and James E. Moore. "Calcium Regulation in Lymphatic Endothelial Cells Under Flow." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14828.

Full text

Abstract:

The lymphatic system collects interstitial fluid and proteins and pumps them back to the blood circulatory system. Additionally, it is important in lipid uptake in the mesentery and immune response. Any failure of the system in pumping lymph results in swelling of tissue and/or organ(s), or lymphedema. The lymphatic system consists of initial lymphatic capillaries and larger collecting vessels. The latter contain tubular regions covered with contracting lymphatic muscle cells, which are separated by bi-leaflet valves to ensure unidirectional flow [1].

APA, Harvard, Vancouver, ISO, and other styles

8

Johnson, G. J., P. C. Dunlop, M. J. Rabiet, L. A. Leis, and AH L. From. "THE DIHYDROPYRIDINE CALCIUM CHANNEL AGONIST, BAY K 8644, AND THE ANTAGONIST, NIFEDIPINE, INHIBIT U46619-INDUCED HUMAN PLATELET ACTIVATION BY COMPETITIVE BINDING TO THE THROMBOXANE A22/PGH2 RECEPTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643756.

Full text

Abstract:

The dihydropyridine (DP) Ca2+ channel antagonist, nifedipine (NF), inhibits platelet aggregation .in vitro and ex vivo by an undefined mechanism. Inhibition of Ca2+ influx via Ca2+ channels is a postulated mechanism, but voltage-dependent Ca2+ channels have not been demonstrated in platelets. We previously observed that NF blocked thromboxane A2 (TXA2)-induced platelet aggregation and secretion. In order to further evaluate the mechanism of DP inhibition of platelet activation, we studied the effects of NF and BAY K 8644, (BAY), a DP with opposite (agonist) effects on muscle cells, on human platelet aggregation and secretion induced by the TXA2 mimic, U46619. We also observed the effects of DP on biochemical consequences of platelet activation: cytoplasmic ionized Ca2+ ([Ca2+]i) by fura-2 fluorescence; phosphorylation of 40,000 Dalton protein (40KP) substrate of protein kinase C by SDS-PAGE and [32p] counting; TXA2 formation by RIA of TXB2. 1μM BAY and 10μM NF inhibited the 2nd wave of platelet aggregation and secretion induced by ADP or epinephrine and blocked aggregation and secretion induced by U46619. A Schild plot gave a slope of -1 indicating competitive inhibition of U46619 by BAY (K1[=0.7μM).BAY and NF also blocked U46619-induced phosphorylation of 40KP, rise in [Ca2+]i and TXB2 formation. The (+)-(R) enantiomer of BAY (BAY+) was responsible for BAY inhibition. BAY, BAY(+), and the R enantiomer of another DP, 202-791, all functioned as competitive antagonists of [3H]-U4661 9 binding (K1[ for BAY=2.8 μM-comparable to known receptor antagonists, 13-azaprostanoic acid and BM 13.177; K1 for BAY(+)=0.69μM). Neither BAY nor NF inhibited[3H]-yohimbine binding to α adrenergic receptors.NF, BAY, BAY(+) and BAY(-) in nM concentrations slightly stimulated platelet aggregation,secretion and biochemical events induced by U46619 similar to their effects on muscle. Therefore, DP's do not inhibit platelet activation by blocking voltage-dependent Ca2+ channels. The mechanism of DP inhibition of TXA2-induced platelet activation is stereoselective, competitive binding to the TXA2/PGH2 receptor. DP's may exert similar effects on TXA2-induced vascular smooth muscle contraction.

APA, Harvard, Vancouver, ISO, and other styles

9

Yim, Peter, George Gallos, Yi Zhang, and Charles W. Emala. "Concomitant Blockade Of Calcium-Activated Chloride Channels (CACC) And Sodium Potassium Chloride Cotransporter (NKCC) Attenuates Acetylcholine Contractions In Human Airway Smooth Muscle." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6033.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Palladino, Joseph L. "Modeling Mouse Soleus Muscle Contraction." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176436.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Calcium in muscle contraction"

1

Westerlind, Kim. Muscle Contraction Arrests Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada572645.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Buck, Edmond. Mechanism of Calcium Release from Skeletal Muscle Sarcoplasmic Reticulum. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1306.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Owen, Laura. Calcium and Redox Control of the Calcium Release Mechanism of Skeletal and Cardiac Muscle Sarcoplasmic Reticulum. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.430.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Stuart, Janice. Chemical Modification of Skeletal Muscle Sarcoplasmic Reticulum Vesicles: A Study of Calcium Permeability. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1388.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Dornan, Thomas. Antioxidant Anthocyanidins and Calcium Transport Modulation of the Ryanodine Receptor of Skeletal Muscle (RyR1). Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.319.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Comeaux, James A., James R. Jauchem, David D. Cox, Carrie C. Crane, and John A. D'Andrea. Muscle Contraction During Electro-Muscular Incapacitation: A Comparison Between Square-Wave Pulses and the Taser (registered trademark) X26 Electronic Control Device. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada597215.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Jalil, Yorschua, and Ruvistay Gutierrez. Myokines secretion and their role in critically ill patients. A scoping review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0048.

Full text

Abstract:

Review question / Objective: 1-How and by which means stimulated muscle from critically ill patients can liberate myokines?, 2-Which are the main characteristics of the critically ill population studied and if some of these influenced myokine´s secretion?, 5-Can myokines exert local or distant effects in critically ill patients?, 5-Which are the potential effects of myokines in critically ill patients? Eligibility criteria: Participants and context: We will include primary studies (randomized or non-randomized trials, observational studies, case series or case report) that consider hospitalized critically ill adult patients (18 years or older) in risk for developing some degree of neuromuscular disorders such as ICU-AW, diaphragmatic dysfunction, or muscle weakness, therefore the specific setting will be critical care. Concept: This review will be focused on studies regarding the secretion or measure of myokines or similar (exerkines, cytokines or interleukin) by any mean of muscle activation or muscle contraction such as physical activity, exercise or NMES, among others. The latter strategies must be understood as any mean by which muscle, and there for myocytes, are stimulated as result of muscle contraction, regardless of the frequency, intensity, time of application and muscle to be stimulated (upper limb, lower limb, thoracic or abdominal muscles). We also will consider myokine´s effects, local or systemic, over different tissues in terms of their structure or function, such as myocytes function, skeletal muscle mass and strength, degree of muscle wasting or myopathies, among others.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!