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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Renzetti, L. M., M. B. Wang, and J. P. Ryan. "Contribution of intracellular calcium to gallbladder smooth muscle contraction." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 1 (July 1, 1990): G1—G5. http://dx.doi.org/10.1152/ajpgi.1990.259.1.g1.
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Studies were performed to evaluate the contribution of intracellular Ca2+ to gallbladder smooth muscle contraction under acetylcholine (ACh) or potassium stimulation. Gallbladder smooth muscle strips from adult guinea pigs were placed in tissue baths containing N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered physiological salt solution (PSS) and set to optimal length for contraction (Lo). The results were as follows, 1) A 20-min equilibration in zero Ca2(+)-0.1 mM ethylene glycol-bis( beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) PSS virtually abolished the response to potassium but not to ACh. 2) Substitution of strontium, an inhibitor of intracellular Ca2+ release, for Ca2+ significantly decreased the contractile response to ACh (3 X 10(-5), 10(-4), and 3 X 10(-4) M). Strontium had no effect on the response to 40 and 80 mM potassium. 3) Intracellular Ca2+ depletion significantly decreased gallbladder smooth muscle contraction to ACh (10(-4) M) but had no effect on the response to potassium (80 mM). 4) Ryanodine, a compound that inhibits Ca2+ storage by the sarcoplasmic reticulum, significantly decreased the contractile response to ACh (10(-4) M) but not to potassium (80 mM). These data support the observation that the use of intracellular Ca2+ by gallbladder smooth muscle for contraction is agonist dependent.
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Podpalova, O. "Muscle contraction dynamics during chronic alcoholization." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 79, no. 3 (2019): 63–68. http://dx.doi.org/10.17721/1728_2748.2019.79.63-68.
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Alcoholic myopathy is considered a multifactorial disease. The mechanisms leading to the development of muscle pathology in the case of excessive alcohol consumption have several implementation options. Chronic alcohol intake and acute alcohol intoxication can reduce the rate of protein synthesis, including myofibrillar proteins, leading to at least 2 functional changes in contractile processes: increased relaxation time and inadequate, incorrect muscle contraction. Chronic alcohol abuse contributes to the impairment of muscle contraction, including the reduction of the force and mechanokinetic parameters of contraction, which may be the result of the ultrastructural organization disruption of myocytes and their atrophy, because ethanol is able to interact directly on membrane structures. Impaired membrane structures and increased Ca2+ -ATPase activity lead to changes in calcium homeostasis and impaired muscle contractile function.Alcohol myopathy is also represents by skeletal muscles weakness, which is caused by a decreasement of the relative weight of myosin, desmin, actin and troponin, titin and nebulin, as ethanol and acetaldehyde act like as potent inhibitors of synthesis of myofibilar and sarcoplasmic proteins. The purpose of the study was to compare the dynamics of the parameters of skeletal muscle contraction of alcoholic rats using electrical stimulation with different relaxation times. In the first series of the experiment, we performed stimulation of m.tibialis rats with electrical pulses of 2.3.4.5 seconds. With a relaxation period of 30 s. In the next series of experiments, we increased the relaxation time to 1 min. in these stimulating conditions, myopathic muscles tend to increase the relaxation time rather than qualitatively or quantitatively change the dynamics of its contractile processes.
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Muinuddin, Ahmad, Leila Neshatian, Herbert Y. Gaisano, and Nicholas E. Diamant. "Calcium source diversity in feline lower esophageal sphincter circular and sling muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 2 (February 2004): G271—G277. http://dx.doi.org/10.1152/ajpgi.00291.2003.
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Within muscular equivalents of cat lower esophageal sphincter (LES), the circular muscle develops greater spontaneous tone, whereas the sling muscle is more responsive to cholinergic stimulation. Smooth muscle contraction involves a combination of calcium release from stores and of calcium entry via several pathways. We hypothesized that there are differences in the sources of Ca2+used for contraction in sling and circular muscles and that these differences could contribute to functional asymmetry observed within LES. Contraction of muscle strips from circular and sling regions of LES was assessed in the presence of TTX. In Ca2+-free Krebs, tone was inhibited to a greater degree in circular than sling muscle. L-type Ca2+channel blockade with nifedipine or verapamil inhibited tone in LES circular but not sling muscle. Sarcoplasmic reticulum (SR) Ca2+-ATPase inhibitor cyclopiazonic acid (CPA) caused greater increase in tone in sling than in circular muscle. The phospholipase C inhibitor U-73122 and the SR inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] receptor blocker 2-aminoethoxydiphenyl borate (2-APB) inhibited tone in circular and sling muscles, demonstrating that continuous release of Ca2+from Ins(1,4,5)P3-sensitive stores is important in tone generation in both muscles. In Ca2+-free Krebs, ACh-induced contractions (AChC) were inhibited to a greater degree in sling than circular muscles. However, nifedipine and verapamil greatly inhibited AChC in the circular but not sling muscle. Depletion of SR Ca2+stores with CPA or inhibition of Ins(1,4,5)P3-mediated store release with either U-73122 or 2-APB inhibited AChC in both muscles. We demonstrate that LES circular and sling muscles 1) use intracellular and extracellular Ca2+sources to different degrees in the generation of spontaneous tone and AChC and 2) use different Ca2+entry pathways. These differences hold the potential for selective modulation of LES tone in health and disease.
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Honoré, E., M. M. Adamantidis, B. A. Dupuis, C. E. Challice, and P. Guilbault. "Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle." Canadian Journal of Physiology and Pharmacology 65, no. 9 (September 1, 1987): 1821–31. http://dx.doi.org/10.1139/y87-284.
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Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.
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Soloviev, A. I., and S. M. Tishkin. "How to measure myofilament calcium sensitivity? Theory and practical applications." Фармакологія та лікарська токсикологія 14, no. 1 (March 27, 2020): 3–14. http://dx.doi.org/10.33250/14.01.003.
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In the heart, as well as in smooth muscle cells (SMC) of blood vessels, contractility is mainly determined by the concentration of free calcium [Ca2+]i. in myoplasm. Changes in the sensitivity of myofilaments to calcium can be very important in the regulation of muscle contractility. Currently, it is precisely this way of influence on the contractile properties of the heart and vascular muscles that attracts much attention of pharmacologists. Studies of the nature of calcium sensitivity can be the fundamental basis for the development of a new generation of drugs that affect vascular tone or contractility of the heart through direct effects on the contractile apparatus or indirectly affecting signaling pathways that regulate vascular tone. The dependence of the magnitude of the contraction F from [Ca2+]i with a good degree of accuracy is described by the Hill equation F = Fmax * [Ca2+]in / (EC50n + [Ca2+]in), which is uniquely determined by three parameters: the maximum contraction Fmax, the concentration of half contraction EC50, and the Hill coefficient n. The main goal of the experiments to determine the changes in the calcium sensitivity of the contractile apparatus of the SMC during any external influences including conducting screening trials of potential drugs should be to obtain the dependencies of the contraction force F on [Ca2+]i. before and after its exposure. To correctly evaluate changes in the calcium sensitivity of myofilaments, it is necessary to measure at least changes in three parameters of the obtained dependences: the generalized affinity of myofilaments for [Ca2+]i, which is characterized as EC50, the sensitivity of myofilaments to calcium, or Fmax, and Hill coefficient. Optimal experimental design for assessing changes in the calcium sensitivity of the vascular contractile apparatus includes: recording the contractile activity of intact smooth muscles, recording the contractile activity of chemically skinned vascular preparations, as well as simultaneously measuring [Ca2+]i, and contractile force using fluorescent calcium indicators. The complex of these experiments will enable a step-by-step assessment of the ability of any external impact, including pharmacological intervention, to change the calcium sensitivity of the contractile apparatus of SMC and can serve as an effective tool for the initial screening of compounds claiming to be calcium sensitizers or desensitizers.
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Eckhardt, Jan, Christoph Bachmann, Marijana Sekulic-Jablanovic, Volker Enzmann, Ki Ho Park, Jianjie Ma, Hiroshi Takeshima, Francesco Zorzato, and Susan Treves. "Extraocular muscle function is impaired in ryr3−/− mice." Journal of General Physiology 151, no. 7 (May 13, 2019): 929–43. http://dx.doi.org/10.1085/jgp.201912333.
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Calcium is an ubiquitous second messenger mediating numerous physiological processes, including muscle contraction and neuronal excitability. Ca2+ is stored in the ER/SR and is released into the cytoplasm via the opening of intracellular inositol trisphosphate receptor and ryanodine receptor calcium channels. Whereas in skeletal muscle, isoform 1 of the RYR is the main channel mediating calcium release from the SR leading to muscle contraction, the function of ubiquitously expressed ryanodine receptor 3 (RYR3) is far from clear; it is not known whether RYR3 plays a role in excitation–contraction coupling. We recently reported that human extraocular muscles express high levels of RYR3, suggesting that such muscles may be useful to study the function of this isoform of the Ca2+ channel. In the present investigation, we characterize the visual function of ryr3−/− mice. We observe that ablation of RYR3 affects both mechanical properties and calcium homeostasis in extraocular muscles. These changes significantly impact vision. Our results reveal for the first time an important role for RYR3 in extraocular muscle function.
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Sommerville, L. E., and D. J. Hartshorne. "Intracellular calcium and smooth muscle contraction." Cell Calcium 7, no. 5-6 (December 1986): 353–64. http://dx.doi.org/10.1016/0143-4160(86)90038-2.
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Röhm, Katrin, Martin Diener, Korinna Huber, and Jana Seifert. "Characterization of Cecal Smooth Muscle Contraction in Laying Hens." Veterinary Sciences 8, no. 6 (May 26, 2021): 91. http://dx.doi.org/10.3390/vetsci8060091.
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The ceca play an important role in the physiology of the gastrointestinal tract in chickens. Nevertheless, there is a gap of knowledge regarding the functionality of the ceca in poultry, especially with respect to physiological cecal smooth muscle contraction. The aim of the current study is the ex vivo characterization of cecal smooth muscle contraction in laying hens. Muscle strips of circular cecal smooth muscle from eleven hens are prepared to investigate their contraction ex vivo. Contraction is detected using an isometric force transducer, determining its frequency, height and intensity. Spontaneous contraction of the chicken cecal smooth muscle and the influence of buffers (calcium-free buffer and potassium-enriched buffer) and drugs (carbachol, nitroprusside, isoprenaline and Verapamil) affecting smooth muscle contraction at different levels are characterized. A decrease in smooth muscle contraction is observed when a calcium-free buffer is used. Carbachol causes an increase in smooth muscle contraction, whereas atropine inhibits contraction. Nitroprusside, isoprenaline and Verapamil result in a depression of smooth muscle contraction. In conclusion, the present results confirm a similar contraction behavior of cecal smooth muscles in laying hens as shown previously in other species.
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Lee, Cheng-Han, Kuo-Hsing Kuo, Jiazhen Dai, and Cornelis van Breemen. "Asynchronous calcium waves in smooth muscle cells." Canadian Journal of Physiology and Pharmacology 83, no. 8-9 (August 1, 2005): 733–41. http://dx.doi.org/10.1139/y05-083.
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Asynchronous Ca2+ waves or wave-like [Ca2+]i oscillations constitute a specialized form of agonist-induced Ca2+ signaling that is observed in a variety of smooth muscle cell types. Functionally, it is involved in the contractile regulation of the smooth muscle cells as it signals for tonic contraction in certain smooth muscle cells while causing relaxation in others. Mechanistically, repetitive Ca2+ waves are produced by repetitive cycles of sarcoplasmic reticulum Ca2+ release followed by Ca2+ uptake. Plasmalemmal Ca2+ entry mechanisms are important for providing the additional Ca2+ necessary to maintain proper refilling of the sarcoplasmic reticulum Ca2+ store and support ongoing Ca2+ waves. In this paper, we will review the phenomenon of asynchronous Ca2+ waves in smooth muscle and discuss the scientific and clinical significance of this new understanding.Key words: excitation-contraction coupling, confocal fluoresence microscopy, calcium signaling.
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Freedman, Stephen M., John L. Wallace, and Eldon A. Shaffer. "Characterization of leukotriene-induced contraction of the guinea-pig gallbladder in vitro." Canadian Journal of Physiology and Pharmacology 71, no. 2 (February 1, 1993): 145–50. http://dx.doi.org/10.1139/y93-020.
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Metabolites of arachidonic acid like prostaglandins have an established role in the pathogenesis of gallstone formation and cholecystitis, but any contribution by leukotrienes is less clear. Leukotrienes might contribute to the disease process by contracting the inflamed and (or) obstructed gallbladder, resulting in further inflammatory damage and biliary pain. To better define the role of leukotrienes, we assessed their effects on gallbladder contracility in vitro. Both leukotriene C4 (LTC4) and D4 (LTD4) had a concentration-dependent excitatory effect on guinea-pig gallbladder smooth muscle. The LTD4-receptor antagonist MK-571 (1 μM) competitively depressed the contractile response, to both LTD4 and LTC4. The source of calcium was defined using ryanodine to deplete intracellular calcium stores and nifedipine to block extracellular entry. Ryanodine (10 μM) antagonized gallbladder contraction at low concentrations of LTD4 (10−10 and 10−9 M). Nifedipine (1 μM) had a greater inhibitory effect on the contractile response at high concentrations of LTD4 (10−8–10−6 M). LTD4-induced contractions were unaffected in tissues pretreated with the neural blocker tetrodotoxin or the muscarinic antagonist atropine. Thus, leukotrienes act directly on the gallbladder smooth muscle, causing contraction at concentrations found in models of cholecystitis, suggesting that these inflammatory mediators contribute to the symptoms and morbidity associated with gallbladder disease.Key words: gallstones, cholecystitis, guinea-pig, gallbladder, leukotriene.
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Francis, B., and C. N. Uchendu. "Extracellular Calcium and Induction of Uterine Muscle Contraction by Aqueous Ethanolic Leaf Extract of Mucuna pruriens." Journal of Applied Sciences and Environmental Management 24, no. 2 (April 16, 2020): 231–35. http://dx.doi.org/10.4314/jasem.v24i2.6.
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Calcium (Ca2+) serves as an essential signaling molecule in biological systems, regulating a wide range of cellular processes of which uterine smooth muscle contraction is among. The present study was designed to evaluate the involvement of Ca2+ on isolated uterine muscle contraction induced by aqueous ethanolic leaf extract of Mucuna pruriens (M. pruriens). Uterine muscle contraction induced by the extract was concentration-dependent and was completely abolished (100%; P<0.05) in nominally Ca2+ -free physiological salt solution and in solutions containing (EGTA 1.5 mmol), lanthanium chloride (1.5 and 3 mmol), caffeine (3and 4.4 mmol) and verapamil (0.007-0.14 μmol). It is concluded that the inability of the extract to produce contractions in Ca2+ -free media, indicates that it lacks the ability to mobilize calcium from intracellular storage sites. Hence, its uterine stimulatory property is therefore solely dependent on extracellular Ca2+.
Keywords: Calcium, Mucuna pruriens, Uterus, Contraction.
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Dangain, Josette, and Ian R. Neering. "Effect of low extracellular calcium and ryanodine on muscle contraction of the mouse during postnatal development." Canadian Journal of Physiology and Pharmacology 69, no. 9 (September 1, 1991): 1294–300. http://dx.doi.org/10.1139/y91-190.
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We have examined the effects of low Ca2+ solutions, Co2+, and ryanodine on the isometric tension and contraction speed of isolated, developing mouse EDL muscles. Twitch responses of young muscles (7–14 days postnatal) were more sensitive to lowered [Ca2+]0 than those of more fully developed muscles (22–35 days postnatal). Responses of EDL muscles from a middle-aged group (15–21 days postnatal) were intermediate between the two other groups. Overall, the time course of contraction in a single twitch was accelerated by low [Ca2+]o. Ca2+-free solution induced a 7.95 and 9.25 mV depolarization in young and "old" muscle fibres, respectively. The presence of cobalt ions (5 mM) in the Krebs solution had a similar effect as Ca2+-free Krebs in terms of reduction of the isometric twitch and tetanic tensions of EDL muscles from the various age groups. In contrast, the shortening of the contraction time seen with Ca2+-free solution did not take place following exposure to Co2+-containing solutions. Finally, young (7–14 days postnatal) muscles were less sensitive to the inhibitory action of ryanodine on the twitch compared with more fully developed muscles (22–35 days postnatal). Taken together, our results indicate that from birth to maturity, there is a gradual change in the spectrum of calcium utilization for the contractile process.Key words: mammalian muscle, calcium, development, ryanodine, contraction, sarcoplasmic reticulum.
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Rondeau, Mark P., Karen Meltzer, Kathryn E. Michel, Catherine M. McManus, and Robert J. Washabau. "Short chain fatty acids stimulate feline colonic smooth muscle contraction." Journal of Feline Medicine and Surgery 5, no. 3 (June 2003): 167–73. http://dx.doi.org/10.1016/s1098-612x(03)00002-0.
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The effect of short chain fatty acids (SCFA) on feline colonic smooth muscle contraction was evaluated in vitro. Colonic tissue was obtained from seven healthy male and female adult cats and seven healthy male and female kittens. Longitudinal and circular colonic smooth muscle strips from proximal and distal colon were incubated with SCFA (acetate, butyrate and propionate; 1–100 mM). SCFA-induced contractions were compared to responses obtained using maximal concentrations (10−4 M) of acetylcholine (ACh). The calcium dependence of the SCFA response was investigated by incubating with nifedipine (1 μM) or verapamil (1 μM). Acetate, butyrate and propionate elicited isometric stress responses (0.25–1.98×104 N/m2) in longitudinal, but not circular, smooth muscle from both the proximal and distal colon of adult cats. Maximal responses were attained at 50 and 100 mM SCFA. Maximal butyrate and propionate responses were 29 and 19% of the maximal ACh response (10−4 M), respectively. Acetate was least effective in stimulating contractile responses. Nifedipine and verapamil abolished all responses. Contractile responses in kittens were similar to those observed in adult cats, but were smaller in amplitude. Results of these studies have shown that SCFA stimulate longitudinal colonic smooth muscle contractions in kittens and adult cats in vitro. These SCFA-induced contractions involve activation of calcium influx. These in vitro findings may account for some of the effects of dietary fiber on feline colonic motility in vivo.
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Knox, Alan J., Paul Ajao, John R. Britton, and Anne E. Tattersfield. "Effect of Sodium-Transport Inhibitors on Airway Smooth Muscle Contractility in Vitro." Clinical Science 79, no. 4 (October 1, 1990): 315–23. http://dx.doi.org/10.1042/cs0790315.
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1. To determine whether alterations in membrane sodium transport in airway smooth muscle can alter its contractility, we studied the effect of ouabain (a Na+/K+-adenosine triphosphatase inhibitor) and amiloride on contractile responses in bovine trachea and human bronchial rings in a series of studies. 2. Ouabain (10−6–10−4 mol/l) caused concentration-related contraction of bovine trachea with a maximum effect at 30 min; the mean increases in tension with 10−6, 10−5 and 10−4 mol/l ouabain were 19, 27, and 32%, respectively, of the maximum response seen with 10−3 mol/l histamine (n = 6). In human bronchial rings, ouabain (10−5 mol/l) caused a mean contraction which was 40% of the maximum response to methacholine (n = 8). 3. Calcium-free fluid (plus ethylenediaminetetra-acetic acid) and nifedipine (10−5 mol/l) inhibited ouabain-induced contractions, suggesting that contraction was mediated in part by calcium entry via voltage-dependent calcium channels. Phentolamine (10−5 mol/l) was without effect. 4. Ouabain (10−5 mol/l) did not alter histamine responsiveness in bovine trachea or methacholine responsiveness in human bronchial rings. 5. Amiloride did not affect resting tone in bovine trachea but caused a concentration-dependent relaxation of bovine tracheal strips preconstricted with carbachol, 10−3 mol/l amiloride relaxing strips completely over 15 minutes (n = 8). Pretreatment with amiloride significantly inhibited contraction produced by both histamine and carbachol in a dose-related manner, 10−5, 10−4 and 10−3 mol/l amiloride shifting the concentration of histamine producing 50% maximal contraction by 3-, 8- and 35-fold (n = 10) and that of carbachol by 1.4-, 6- and 86-fold (n = 8), respectively. 6. Amiloride also reduced the contraction produced by 10−4 mol/l ouabain from 32% (control) to 7% of the maximum histamine response. 7. Our results suggest that alterations in cell membrane sodium transport modify the contractile properties of airway smooth muscle.
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Walsh, Michael P. "Calcium-dependent mechanisms of regulation of smooth muscle contraction." Biochemistry and Cell Biology 69, no. 12 (December 1, 1991): 771–800. http://dx.doi.org/10.1139/o91-119.
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The contractile state of smooth muscle is regulated primarily by the sarcoplasmic (cytosolic) free Ca2+ concentration. A variety of stimuli that induce smooth muscle contraction (e.g., membrane depolarization, α-adrenergic and muscarinic agonists) trigger an increase in sarcoplasmic free [Ca2+] from resting levels of 120–270 to 500–700 nM. At the elevated [Ca2+], Ca2+ binds to calmodulin, the ubiquitous and multifunctional Ca2+-binding protein. The interaction of Ca2+ with CaM induces a conformational change in the Ca2+-binding protein with exposure of a site(s) of interaction with target proteins, the most important of which in the context of smooth muscle contraction is the enzyme myosin light chain kinase. The interaction of calmodulin with myosin light chain kinase results in activation of the kinase that catalyzes phosphorylation of myosin at serine-19 of each of the two 20-kDa light chains (native myosin is a hexamer composed of two heavy chains (230 kDa each) and two pairs of light chains (one pair of 20 kDa each and the other pair of 17 kDa each)). This simple phosphorylation reaction triggers cycling of myosin cross-bridges along actin filaments and the development of force. Relaxation of the muscle follows removal of Ca2+ from the sarcoplasm, whereupon calmodulin dissociates from myosin light chain kinase regenerating the inactive kinase; myosin is dephosphorylated by myosin light chain phosphatase(s), whereupon it dissociates and remains detached from the actin filament and the muscle relaxes. A substantial body of evidence has been accumulated in support of this central role of myosin phosphorylation–dephosphorylation in the regulation of smooth muscle contraction. However, a wide range of physiological and biochemical studies supports the existence of additional, secondary Ca2+-dependent mechanisms that can modulate or fine-tune the contractile state of the smooth muscle cell. Three such mechanisms have emerged: (i) the actin-, tropomyosin-, and calmodulin-binding protein, calponin; (ii) the actin-, myosin-, tropomyosin-, and calmodulin-binding protein, caldesmon; and (iii) the Ca2+- and phospholipid-dependent protein kinase (protein kinase C).Key words: smooth muscle, Ca2+, myosin phosphorylation, regulation of contraction.
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Adams, B. A., and K. G. Beam. "Contractions of dysgenic skeletal muscle triggered by a potentiated, endogenous calcium current." Journal of General Physiology 97, no. 4 (April 1, 1991): 687–96. http://dx.doi.org/10.1085/jgp.97.4.687.
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The dihydropyridine (DHP) receptor of normal skeletal muscle is hypothesized to function as the voltage sensor for excitation-contraction (E-C) coupling, and also as the calcium channel underlying a slowly activating, DHP-sensitive current (termed ICa-s). Skeletal muscle from mice with muscular dysgenesis lacks both E-C coupling and ICa-s. However, dysgenic skeletal muscle does express a small DHP-sensitive calcium current (termed ICa-dvs) which is kinetically and pharmacologically distinct from ICa-s. We have examined the ability of ICa-dys, or the DHP receptor underlying it, to couple depolarization and contraction. Under most conditions ICa-dys is small (approximately 1 pA/pF) and dysgenic myotubes do not contract in response to sarcolemmal depolarization. However, in the combined presence of the DHP agonist Bay K 8644 (1 microM) and elevated external calcium (10 mM), ICa-dys is strongly potentiated and some dysgenic myotubes contract in response to direct electrical stimulation. These contractions are blocked by removing external calcium, by adding 0.5 mM cadmium to the bath, or by replacing Bay K 8644 with the DHP antagonist (+)-PN 200-110. Only myotubes having a density of ICa-dys greater than approximately 4 pA/pF produce detectible contractions, and the strength of contraction is positively correlated with the density of ICa-dys. Thus, unlike the contractions of normal myotubes, the contractions of dysgenic myotubes require calcium entry. These results demonstrate that the DHP receptor underlying ICa-dys is unable to function as a "voltage sensor" that directly couples membrane depolarization to calcium release from the sarcoplasmic reticulum.
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Akata, Takashi, and Walter A. Boyle. "Dual Actions of Halothane on Intracellular Calcium Stores of Vascular Smooth Muscle." Anesthesiology 84, no. 3 (March 1, 1996): 580–95. http://dx.doi.org/10.1097/00000542-199603000-00014.
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Background Halothane has been reported to affect the integrity of intracellular Ca2+ stores in a number of tissues including vascular smooth muscle. However, the actions of halothane on intracellular Ca2+ stores are not yet fully understood. Methods Employing the isometric tension recording method, the action of halothane in isolated endothelium-denuded rat mesenteric arteries under either intact or beta-escinmembrane-permeabilized conditions was investigated. Results Halothane (0.125-5%) produced concentration-dependent contractions in Ca2+ free solution in both intact and membrane-permeabilized muscle strips. Ryanodine treatment or repetitive application of phenylephrine eliminated both caffeine-and halothane-induced contractions in the Ca2+ free solution. When either halothane and caffeine, caffeine and halothane, phenylephrine and halothane, or inositol 1,4,5-triphosphate and halothane were applied consecutively in the Ca2+ free solution in either intact or membrane-permeabilized muscle strips, the contraction induced by application of the second agent of the pair was inhibited compared to application of that agent alone. However, when procaine was applied before and during application of the first agent, the contraction induced by the first agent was inhibited and the contraction induced by the second agent was restored. Heparin inhibited the inositol 1,4,5-triphosphate-mediated contraction, but not contractions induced by halothane or caffeine. Halothane (0.125-5%), applied during Ca2+ loading, produced concentration-dependent inhibition of the caffeine contraction (used to estimate the amount of Ca2+ in the store) in both intact and membrane-permeabilized muscle strips. In contrast, halothane applied with procaine during Ca2+ loading produced concentration-dependent enhancement of the caffeine contraction. This enhancement was observed only in the intact but not in the membrane-permeabilized condition. Conclusions Halothane has two distinct actions on the intracellular Ca2+ stores of vascular smooth muscle, a Ca2+ releasing action and a stimulating action on Ca2+ uptake. Halothane releases Ca2+ from the stores that are sensitive to both caffeine/ryanodine and phenylephrine/inositol 1,4,5-triphosphate through a procaine-sensitive mechanism. The observed inhibitory effect on Ca2+ uptake is probably caused by the Ca2+ uptake after blockade of Ca2+ release may be membrane-mediated.
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Bitar, K. N., G. M. Burgess, J. W. Putney, and G. M. Makhlouf. "Source of activator calcium in isolated guinea pig and human gastric muscle cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 3 (March 1, 1986): G280—G286. http://dx.doi.org/10.1152/ajpgi.1986.250.3.g280.
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The source of Ca2+ responsible for contraction was examined in suspensions of smooth muscle cells and in perfused single muscle cells from guinea pig and human stomach. In both preparations removal of Ca2+ from the medium or addition of the Ca2+ channel blocker methoxyverapamil had no effect on the contractile response to various agonists, including cholecystokinin octapeptide (CCK-8) and acetylcholine, but inhibited the response to high extracellular K+ by 76-82%. Repeated stimulation of guinea pig or human single muscle cells in Ca2+-free medium, or in the presence of methoxyverapamil caused a progressive decrease and eventual abolition of contractile response; response was restored on restitution of Ca2+ to the medium or elimination of methoxyverapamil. Measurement of 45Ca2+ content in guinea pig muscle cells showed that CCK-8 had no effect on the rate of Ca2+ influx but increased the rate of Ca2+ efflux transiently by sixfold. Net peak efflux coincided with the time of peak contraction and was stoichiometrically related to the degree of contraction. Equipotent, maximally effective contractile doses of CCK-8, acetylcholine, and methionine-enkephalin caused equivalent degrees of net Ca2+ efflux. The results indicate that contractile agonists cause release of Ca2+ from a depletable intracellular store in gastric muscle cells. The release is accompanied by a dose-dependent increase in Ca2+ efflux and is capable of sustaining an initial maximal contraction. Repeated contractile activity requires influx of Ca2+ from extracellular sources.
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Moravec, C. S., and M. Bond. "Calcium is released from the junctional sarcoplasmic reticulum during cardiac muscle contraction." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 3 (March 1, 1991): H989—H997. http://dx.doi.org/10.1152/ajpheart.1991.260.3.h989.
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We have used electron-probe microanalysis (EPMA) to address the question of Ca2+ release by junctional sarcoplasmic reticulum (JSR) as well as Ca2+ regulation by mitochondria (MT) during cardiac muscle contraction. Hamster papillary muscles were rapidly frozen during relaxation or at the peak rate of tension rise (+dT/dt). Total Ca2+ content was measured by EPMA in the JSR, within a MT, over the A band, and in the whole cell, in nine cells per animal (five animals per group). JSR Ca2+ content was found to be significantly lower in muscles frozen at the peak of contraction [7.3 +/- 1.3 (mean +/- SE) mmol Ca2+/kg dry wt] than in those frozen during relaxation (12.5 +/- 1.9 mmol Ca2+/kg dry wt; P less than 0.01), suggesting that Ca2+ is released from this storage site during cardiac muscle contraction. In contrast, MT Ca2+ content did not change significantly during contraction (0.4 +/- 0.1 mmol/kg dry wt) compared with relaxation (0.1 +/- 0.2 mmol/kg dry wt). A third group of muscles was frozen during relaxation after pretreatment with 10(-7) M ryanodine. Ca2+ content of the JSR was significantly decreased (P less than 0.01) in this group of muscles, (6.4 +/- 1.8 mmol/kg dry wt) compared with those frozen during relaxation in the absence of the drug. This suggests that the intracellular storage site with a decreased Ca2+ content in muscles frozen at the peak of contraction is the ryanodine-releasable store. These results provide the first direct measurement of the Ca2+ content of both JSR and MT during a normal cardiac muscle contraction and demonstrate that Ca2+ is released from the JSR during muscle contraction.
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Walsh, Michael P., Jacquelyn E. Andrea, Bruce G. Allen, Odile Clément-Chomienne, Elizabeth M. Collins, and Kathleen G. Morgan. "Smooth muscle protein kinase C." Canadian Journal of Physiology and Pharmacology 72, no. 11 (November 1, 1994): 1392–99. http://dx.doi.org/10.1139/y94-201.
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Protein kinase C (PKC) was first implicated in the regulation of smooth muscle contraction with the observation that phorbol esters induce slowly developing, sustained contractions. In some vascular smooth muscles, e.g., ferret aorta, phorbol ester induced contractions occur without an increase in sarcoplasmic free-Ca2+ concentration ([Ca]i) or myosin light chain phosphorylation. This response appears to be mediated by a Ca2+-independent isoenzyme of PKC (probably PKCε), since saponin-permeabilized single ferret aortic smooth muscle cells, which retain receptor coupling, developed force in response to phenylephrine at low free [Ca2+] (pCa 7.0–8.6) and the constitutively active proteolytic fragment of PKC (PKM) elicited a contraction at pCa 7 comparable with the phenylephrine-induced contraction. Both contractions were reversed by a pseudo-substrate peptide inhibitor of PKC. These observations suggest a mechanism whereby α-adrenergic agonists may elicit a contractile response without a Ca2+ signal: α-adrenergic stimulation of phosphatidylcholine-specific phosphoiipase C or D (the latter in conjunction with phosphatidate phosphohydrolase) generates diacylglycerol. In the absence of an increase in [Ca2+]i, diacylglycerol specifically activates so-called novel PKCs, of which ε is the only isoenzyme known to be expressed in vascular smooth muscle. Recent evidence suggests that PKC may trigger a cascade of phosphorylation reactions, resulting in activation of mitogen-activated protein kinase and phosphorylation of the thin filament associated protein caldesmon. Alternatively, or additionally, PKC may directly phosphorylate calponin, another thin filament associated protein. These phosphorylations are predicted to alleviate inhibition of the cross-bridge cycling rate by these thin-filament proteins. The slow development of force would then result from a slow rate of cross-bridge cycling due to the low basal level of myosin phosphorylation.Key words: protein kinase C, smooth muscle, calcium, caldesmon, calponin.
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Cognard, C., B. Constantin, M. Rivet-Bastide, N. Imbert, C. Besse, and G. Raymond. "Appearance and evolution of calcium currents and contraction during the early post-fusional stages of rat skeletal muscle cells developing in primary culture." Development 117, no. 3 (March 1, 1993): 1153–61. http://dx.doi.org/10.1242/dev.117.3.1153.
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Primary cultures from enzymatically dissociated satellite cells of newborn rat skeletal muscles enabled developmental in vitro studies of mechanical and electrical properties during the first steps of myogenesis. The present work focused on the appearance, evolution and roles of two types of calcium currents (ICa,T and ICa,L) and of depolarization-induced contractile activity during the early stages of muscle cell development in primary culture. Prefusional mononucleated cells (myoblasts), young myotubes of 1 day (with less than 10 nuclei) or 2–3 days (more than 9 nuclei) and myoballs from 4–6, 7–9, 10–12 and 13–16 days cultures were patch-clamped (whole-cell configuration), and calcium currents and contraction simultaneously recorded. Sodium but not calcium currents could be recorded at the myoblast stage. In young myotubes (1 day), ICa,L was present with high incidence as compared to ICa,T, which was poorly expressed. Contractile responses appeared at the next stage (2-3 days) while the occurrence of ICa,T progressively increased. This developmental evolution of the calcium currents and contraction expression was accompanied by some changes in their characteristics: the ICa,T/ICa,L amplitudes ratio progressively increased and the time-to-peak of contraction progressively decreased with the age of myoballs. Physiological functions for calcium currents in developing muscle are suggested and discussed: ICa,T, which is transiently expressed, could be involved in the pacemaker-like activity while ICa,L could serve as an early contraction triggering mechanism and/or initially to fill and then to maintain the intracellular calcium stores.
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Yu, S. N., P. E. Crago, and H. J. Chiel. "A nonisometric kinetic model for smooth muscle." American Journal of Physiology-Cell Physiology 272, no. 3 (March 1, 1997): C1025—C1039. http://dx.doi.org/10.1152/ajpcell.1997.272.3.c1025.
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We have modeled the nonisometric contractile dynamics of smooth muscle by modifying a four-state model of actin and myosin bonds originally proposed by Hai and Murphy to simulate the isometric contractions of vertebrate smooth muscle. The model includes a latch bridge, which cycles more slowly than regular cross bridges. We generalized this model to represent the calcium-regulated processes of vertebrate and invertebrate smooth muscles. We added length dynamics by assuming length-dependent bonding and unbonding rates for the cross bridges. The calculation of the cross-bridge length distribution was simplified by assuming a Gaussian distribution, as first done by Zahalak for skeletal muscle. To test the performance of this model, we simulated isometric and nonisometric responses of different kinds of smooth muscle, including vascular smooth muscle, airway smooth muscle, molluscan catch muscle (anterior byssus retractor muscle), and Aplysia I(2) muscle. The model captures the economical force maintenance property at the later stages of isometric muscle contraction and responses to imposed lengthening and shortening movements.
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Wright, David C., Paige C. Geiger, Dong-Ho Han, and John O. Holloszy. "Are tyrosine kinases involved in mediating contraction-stimulated muscle glucose transport?" American Journal of Physiology-Endocrinology and Metabolism 290, no. 1 (January 2006): E123—E128. http://dx.doi.org/10.1152/ajpendo.00280.2005.
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Muscle contractions and insulin stimulate glucose transport into muscle by separate pathways. The contraction-mediated increase in glucose transport is mediated by two mechanisms, one involves the activation of 5′-AMP-activated protein kinase (AMPK) and the other involves the activation of calcium/calmodulin-dependent protein kinase II (CAMKII). The steps leading from the activation of AMPK and CAMKII to the translocation of GLUT4 to the cell surface have not been identified. Studies with the use of the tyrosine kinase inhibitor genistein suggest that one or more tyrosine kinases could be involved in contraction-stimulated glucose transport. The purpose of the present study was to determine the involvement of tyrosine kinases in contraction-stimulated glucose transport in rat soleus and epitrochlearis muscles. Contraction-stimulated glucose transport was completely prevented by pretreatment with genistein (100 μM) and the related compound butein (100 μM). However, the structurally distinct tyrosine kinase inhibitors 4-amino-5-(4-chlorophenyl)-7-( t-butyl)pyrazolo[3,4-d]pyridine and herbimycin did not reduce contraction-stimulated glucose transport. Furthermore, genistein and butein inhibited glucose transport even when muscles were exposed to these compounds after being stimulated to contract. Muscle contractions did not result in increases in tyrosine phosphorylation of proteins such as proline-rich tyrosine kinase and SRC. These results provide evidence that tyrosine kinases do not mediate contraction-stimulated glucose transport and that the inhibitory effects of genistein on glucose transport result from direct inhibition of the glucose transporters at the cell surface.
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Sevy, N., and W. J. Snape. "Sources of calcium for contraction of distal circular muscle or taenia coli in the rabbit." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 6 (June 1, 1988): G808—G813. http://dx.doi.org/10.1152/ajpgi.1988.254.6.g808.
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Studies were performed on proximal taenia coli and distal circular muscle from the rabbit to determine if the source of Ca2+ required for bethanechol stimulation of contraction was similar after permeabilizing the tissues with saponin. The EC50 for Ca2+ stimulation of contraction was pCa 6.1 +/- 0.1 for both tissues. The peak response occurred at pCa 4.5. The addition of 1 microM calmodulin did not alter the Ca2+ EC50 or the peak response. Caffeine (20 mM) stimulated contraction of both taenia coli and distal circular muscle. The caffeine-stimulated contractile response was threefold greater in the taenia than in the distal circular muscle (P less than 0.05). Perfusion of thin strips of colonic muscle with buffer, containing 10(-7) M Ca2+, reduced the amplitude of bethanechol-stimulated contraction. The perfusion time to reduce the contraction by 50% was greater in the proximal muscle (2.4 +/- 0.1 min) than in the distal muscle (1.1 +/- 0.5 min) (P less than 0.001). These data suggest that 1) the intracellular Ca2+ concentration necessary for contraction is similar in the proximal and distal colon and 2) the intracellular Ca2+ stores appear to be greater in proximal taenia coli compared with distal circular muscle.
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Curtis, B. A., and R. S. Eisenberg. "Calcium influx in contracting and paralyzed frog twitch muscle fibers." Journal of General Physiology 85, no. 3 (March 1, 1985): 383–408. http://dx.doi.org/10.1085/jgp.85.3.383.
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Calcium uptake produced by a potassium contracture in isolated frog twitch fibers was 6.7 +/- 0.8 pmol in 0.7 cm of fiber (mean +/- SEM, 21 observations) in the presence of 30 microM D600. When potassium was applied to fibers paralyzed by the combination of 30 microM D600, cold, and a prior contracture, the calcium uptake fell to 3.0 +/- 0.7 pmol (11): the fibers were soaked in 45Ca in sodium Ringer for 3 min before 45Ca, in a potassium solution, was added for 2 min; each estimate of uptake was corrected for 5 min of resting influx, measured from the same fiber (average = 2.3 +/- 0.3 pmol). The calcium influx into paralyzed fibers is unrelated to contraction. This voltage-sensitive, slowly inactivating influx, which can be blocked by 4 mM nickel, has properties similar to the calcium current described by several laboratories. The paired difference in calcium uptake between contracting and paralyzed fibers, 2.9 +/- 0.8 pmol (16), is a component of influx related to contraction. Its size varies with contracture size and it occurs after tension production: 45Ca applied immediately after contracture is taken up in essentially the same amounts as 45Ca added before contraction. This delayed uptake is probably a "reflux" refilling a binding site on the cytoplasmic side of the T membrane, which had been emptied during the prior contracture, perhaps to initiate it. We detect no component of calcium uptake related to excitation-contraction coupling occurring before or during a contracture.
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Ikegami, Ryo, Hiroaki Eshima, Takuro Mashio, Tomosada Ishiguro, Daisuke Hoshino, David C. Poole, and Yutaka Kano. "Accumulation of intramyocyte TRPV1-mediated calcium during heat stress is inhibited by concomitant muscle contractions." Journal of Applied Physiology 126, no. 3 (March 1, 2019): 691–98. http://dx.doi.org/10.1152/japplphysiol.00668.2018.
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Heat stress promotes intramyocyte calcium concentration ([Ca2+]i) accumulation via transient receptor potential vanilloid 1 (TRPV1) channels. We tested the hypothesis that muscle contractile activity concomitant with heat stress would accelerate the increase in [Ca2+]i via TRPV1, further impairing [Ca2+]i homeostasis. Spinotrapezius muscles of adult Wistar rats were exteriorized in vivo and loaded with the fluorescent Ca2+ probe fura 2-AM. Heat stress (muscle surface temperature 40°C) was used as TRPV1 activator. An isometric contraction (100 Hz, 5–10 V, 30 s) was induced electrically concomitant with heat stress. [Ca2+]i was determined for 20 min using in vivo fluorescence microscopy, and the phosphorylation response of TRPV1 was determined by Western blotting. Heat stress induced a significant [Ca2+]i increase of 18.5 ± 8.1% at 20 min and TRPV1 phosphorylation (+231%), which was inhibited by addition of the TRPV1 inhibitor (capsazepine). However, contrary to expectations, the heat stress and isometric contraction condition almost completely inhibited TRPV1 phosphorylation and the consequent [Ca2+]i elevation (<2.8% accumulation during heat stress, P > 0.05). In conclusion, this in vivo physiological model demonstrated that isometric muscle contraction(s) can suppress the phosphorylation response of TRPV1 and maintain [Ca2+]i homeostasis during heat stress. NEW & NOTEWORTHY This investigation is the first document the dynamics of intramyocyte calcium concentration ([Ca2+]i) increase in the myoplasm of skeletal muscle fibers in response to heat stress where the muscle blood flow is preserved. Heat stress at 40°C drives a myoplasmic [Ca2+]i accumulation in concert with transient receptor potential vanilloid 1 (TRPV1) phosphorylation. However, muscle contraction caused TRPV1 channel deactivation by dephosphorylation of TRPV1. TRPV1 inactivation via isometric contraction(s) permits maintenance of [Ca2+]i homeostasis even under high imposed muscle temperature.
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Booth, John, Michael J. McKenna, Patricia A. Ruell, Tom H. Gwinn, Glen M. Davis, Martin W. Thompson, Alison R. Harmer, Sandra K. Hunter, and John R. Sutton. "Impaired calcium pump function does not slow relaxation in human skeletal muscle after prolonged exercise." Journal of Applied Physiology 83, no. 2 (August 1, 1997): 511–21. http://dx.doi.org/10.1152/jappl.1997.83.2.511.
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Booth, John, Michael J. McKenna, Patricia A. Ruell, Tom H. Gwinn, Glen M. Davis, Martin W. Thompson, Alison R. Harmer, Sandra K. Hunter, and John R. Sutton. Impaired calcium pump function does not slow relaxation in human skeletal muscle after prolonged exercise. J. Appl. Physiol. 83(2): 511–521, 1997.—This study examined the effects of prolonged exercise on human quadriceps muscle contractile function and homogenate sarcoplasmic reticulum Ca2+ uptake and Ca2+-adenosinetriphosphatase activity. Ten untrained men cycled at 75 ± 2% (SE) peak oxygen consumption until exhaustion. Biopsies were taken from the right vastus lateralis muscle at rest, exhaustion, and 20 and 60 min postexercise. Peak tension and half relaxation time of the left quadriceps muscle were measured during electrically evoked twitch and tetanic contractions and a maximal voluntary isometric contraction at rest, exhaustion, and 10, 20, and 60 min postexercise. At exhaustion, homogenate Ca2+ uptake and Ca2+ adenosinetriphosphatase activity were reduced by 17 ± 4 and 21 ± 5%, respectively, and remained depressed after 60 min recovery ( P ≤ 0.01). Muscle ATP, creatine phosphate, and glycogen were all depressed at exhaustion ( P ≤ 0.01). Peak tension during a maximal voluntary contraction, a twitch, and a 10-Hz stimulation were reduced after exercise by 28 ± 3, 45 ± 6, 65 ± 5%, respectively ( P ≤ 0.01), but no slowing of half relaxation times were found. Thus fatigue induced by prolonged exercise reduced muscle Ca2+ uptake, but this did not cause a slower relaxation of evoked contractions.
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Honoré, E., C. E. Challice, P. Guilbault, and B. Dupuis. "Two components of contraction in guinea pig papillary muscle." Canadian Journal of Physiology and Pharmacology 64, no. 9 (September 1, 1986): 1153–59. http://dx.doi.org/10.1139/y86-196.
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Biphasic contractions were produced in guinea pig papillary muscle by inducing partial depolarization in a K+-rich solution (22 mM) containing 10−6 M isoproterenol. However, when the same conditions were applied to frog and rat, monophasic contractions were obtained. In the case of guinea pig, an increase in the beating frequency produced an increase in amplitude of the first component and a reduction of the second, while in frog and rat, only a decrease in the amplitude of contractions was recorded. Caffeine (10−3 M) eliminated the first component and increased the second in guinea pig, while in the case of rat and frog it decreased the amplitude of contractions. Procaine (10−3 M) suppressed the first component and decreased the second one. The contraction in frog appears to be similar to the second component of contraction in guinea pig, while in rat, the contraction is comparable with the first component in guinea pig. It is suggested that the calcium ions which activate the two components of contraction in guinea pig under the given experimental conditions may arise from two different sources.
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Pfitzer, G. "16 Calcium and vascular smooth muscle contraction." Pediatric Research 20, no. 10 (October 1986): 1036. http://dx.doi.org/10.1203/00006450-198610000-00070.
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Yoshimura, Yasukuni, and Osamu Yamaguchi. "Calcium Independent Contraction of Bladder Smooth Muscle." International Journal of Urology 4, no. 1 (January 1997): 62–67. http://dx.doi.org/10.1111/j.1442-2042.1997.tb00142.x.
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Oakley, Carlee I., Julian A. Vallejo, Derek Wang, Mark A. Gray, LeAnn M. Tiede-Lewis, Tilitha Shawgo, Emmanuel Daon, George Zorn, Jason R. Stubbs, and Michael J. Wacker. "Trimethylamine-N-oxide acutely increases cardiac muscle contractility." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 5 (May 1, 2020): H1272—H1282. http://dx.doi.org/10.1152/ajpheart.00507.2019.
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We demonstrate for the first time that elevated concentrations of TMAO acutely augment myocardial contractile force ex vivo in both murine and human cardiac tissue. To gain mechanistic insight into the processes that led to this potentiation in cardiac contraction, we used two-photon microscopy to evaluate intracellular calcium in ex vivo whole hearts loaded with the calcium indicator dye Fluo-4. Acute treatment with TMAO resulted in increased Fluo-4 fluorescence, indicating that augmented cytosolic calcium plays a role in the effects of TMAO on force production. Lastly, TMAO did not show an effect on aortic smooth muscle contraction or relaxation properties. Our results demonstrate novel, acute, and direct actions of TMAO on cardiac function and help lay the groundwork for future translational studies investigating the complex multiorgan interplay involved in cardiovascular pathogenesis during CKD.
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Tabuchi, Ayaka, Hiroaki Eshima, Yoshinori Tanaka, Shunsuke Nogami, Naoki Inoue, Mizuki Sudo, Hidetaka Okada, David C. Poole, and Yutaka Kano. "Regional differences in Ca2+ entry along the proximal-middle-distal muscle axis during eccentric contractions in rat skeletal muscle." Journal of Applied Physiology 127, no. 3 (September 1, 2019): 828–37. http://dx.doi.org/10.1152/japplphysiol.01005.2018.
Full textAbstract:
Eccentric (ECC) contraction-induced muscle damage is associated with calcium ion (Ca2+) influx from the extracellular milieu through stretch-activated channels. It remains unknown whether Ca2+ influx consequent to repetitive ECC contractions is nonuniform across different muscle regions. We tested the hypothesis that there are regional differences in Ca2+ entry along the proximal-middle-distal muscle axis. Tibialis anterior (TA) muscles of adult male Wistar rats were exposed by reflecting the overlying skin and fasciae and ECC contractions evoked by peroneal nerve stimulation paired with simultaneous ankle extension (50 times/set, 2 protocols: 1 set and 10 sets). During ECC in the proximal, middle, and distal TA, we determined 1) muscle fiber extension by high-speed camera (200 frames/s) and 2) Ca2+ accumulation by in vivo bioimaging (Ca2+-sensitive probe Fura-2-acetoxymethyl ester). Muscle fiber extension from resting was significantly different among regions (i.e., proximal, 4.0%: < middle, 11.2%: < distal, 17.0%; ECC phase length at 500th contraction). Intracellular Ca2+ accumulation after 1 set of ECC was higher in the distal (1.46 ± 0.04, P < 0.05) than the proximal (1.27 ± 0.04) or middle (1.26 ± 0.05) regions. However, this regional Ca2+ accumulation difference disappeared by 32.5 min after the 1 set protocol when the muscle was quiescent and by contraction set 5 for the 10-set protocol. The initial preferential ECC-induced Ca2+ accumulation observed distally was associated spatially with the greater muscle extension compared with that of the proximal and middle regions. Disappearance of the regional Ca2+ accumulation disparity in quiescent and ECC-contracting muscle might be explained, in part, by axial Ca2+ propagation and account for the uniformity of muscle damage across regions evident 3 days post-ECC. NEW & NOTEWORTHY After 1 set of 50 eccentric (ECC) contractions in the anterior tibialis muscle, intracellular Ca2+ ([Ca2+]i) accumulation evinces substantial regional heterogeneity that is spatially coherent with muscle length changes (i.e., distal [Ca2+]i > middle, proximal). However, irrespective of whether 50 or 500 ECC contractions are performed, this heterogeneity is subsequently abolished, at least in part, by axial intracellular Ca2+ propagation. This Ca2+ homogenization across regions is consistent with the absence of any interregional difference in muscle damage 3 days post-ECC.
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Lake, N., J. B. Splawinski, C. Juneau, and J. L. Rouleau. "Effects of taurine depletion on intrinsic contractility of rat ventricular papillary muscles." Canadian Journal of Physiology and Pharmacology 68, no. 7 (July 1, 1990): 800–806. http://dx.doi.org/10.1139/y90-122.
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Contractile parameters in Krebs–Henseleit media containing various calcium concentrations were compared in left ventricular papillary muscles of two groups of rats: control and taurine depleted. All tests were carried out with the muscles at initial length, Lmax, the length that produced maximal active tension. From measurements of after- and un-loaded contractions, the velocity–tension curves and the derived maximum velocity of shortening were not different between the groups. Time to peak shortening and extent of shortening were not altered, while relaxation times and contraction duration were significantly prolonged for taurine-depleted muscles. Peak isometric tension and its rate of development were significantly reduced in taurine-depleted muscles compared with controls. Postrest (3 min) stimuli and paired stimuli (200-ms interval) evoked similar potentiated contractile responses in both groups, such that the ratio of their peak tensions remained unchanged. For taurine-depleted muscles the force-frequency relationship (a negative staircase) was parallel to, but lower than, control. These experiments suggest that taurine deficiency leads to reductions in action potential triggered calcium release from internal stores, and deficits in calcium sequestration. This may result from disfacilitation of calcium binding to the sarcoplasmic reticulum and other storage sites during taurine deficiency.Key words: taurine depletion, rat papillary muscle contractility.
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Wright, David C., Paige C. Geiger, John O. Holloszy, and Dong-Ho Han. "Contraction- and hypoxia-stimulated glucose transport is mediated by a Ca2+-dependent mechanism in slow-twitch rat soleus muscle." American Journal of Physiology-Endocrinology and Metabolism 288, no. 6 (June 2005): E1062—E1066. http://dx.doi.org/10.1152/ajpendo.00561.2004.
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Increases in contraction-stimulated glucose transport in fast-twitch rat epitrochlearis muscle are mediated by AMPK- and Ca2+/calmodulin-dependent protein kinase (CAMK)-dependent signaling pathways. However, recent studies provide evidence suggesting that contraction-stimulated glucose transport in slow-twitch skeletal muscle is mediated through an AMPK-independent pathway. The purpose of the present study was to test the hypothesis that contraction-stimulated glucose transport in rat slow-twitch soleus muscle is mediated by an AMPK-independent/Ca2+-dependent pathway. Caffeine, a sarcoplasmic reticulum (SR) Ca2+-releasing agent, at a concentration that does not cause muscle contractions or decreases in high-energy phosphates, led to an ∼2-fold increase in 2-deoxyglucose (2-DG) uptake in isolated split soleus muscles. This increase in glucose transport was prevented by the SR calcium channel blocker dantrolene and the CAMK inhibitor KN93. Conversely, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR), an AMPK activator, had no effect on 2-DG uptake in isolated split soleus muscles yet resulted in an ∼2-fold increase in the phosphorylation of AMPK and its downstream substrate acetyl-CoA carboxylase. The hypoxia-induced increase in 2-DG uptake was prevented by dantrolene and KN93, whereas hypoxia-stimulated phosphorylation of AMPK was unaltered by these agents. Tetanic muscle contractions resulted in an ∼3.5-fold increase in 2-DG uptake that was prevented by KN93, which did not prevent AMPK phosphorylation. Taken in concert, our results provide evidence that hypoxia- and contraction-stimulated glucose transport is mediated entirely through a Ca2+-dependent mechanism in rat slow-twitch muscle.
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Fredsted, Anne, Hanne Gissel, Klavs Madsen, and Torben Clausen. "Causes of excitation-induced muscle cell damage in isometric contractions: mechanical stress or calcium overload?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 6 (June 2007): R2249—R2258. http://dx.doi.org/10.1152/ajpregu.00415.2006.
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Prolonged or unaccustomed exercise leads to muscle cell membrane damage, detectable as release of the intracellular enzyme lactic acid dehydrogenase (LDH). This is correlated to excitation-induced influx of Ca2+, but it cannot be excluded that mechanical stress contributes to the damage. We here explore this question using N-benzyl- p-toluene sulfonamide (BTS), which specifically blocks muscle contraction. Extensor digitorum longus muscles were prepared from 4-wk-old rats and mounted on holders for isometric contractions. Muscles were stimulated intermittently at 40 Hz for 15–60 min or exposed to the Ca2+ ionophore A23187. Electrical stimulation increased 45Ca influx 3–5 fold. This was followed by a progressive release of LDH, which was correlated to the influx of Ca2+. BTS (50 μM) caused a 90% inhibition of contractile force but had no effect on the excitation-induced 45Ca influx. After stimulation, ATP and creatine phosphate levels were higher in BTS-treated muscles, most likely due to the cessation of ATP-utilization for cross-bridge cycling, indicating a better energy status of these muscles. No release of LDH was observed in BTS-treated muscles. However, when exposed to anoxia, electrical stimulation caused a marked increase in LDH release that was not suppressed by BTS but associated with a decrease in the content of ATP. Dynamic passive stretching caused no increase in muscle Ca2+ content and only a minor release of LDH, whereas treatment with A23187 markedly increased LDH release both in control and BTS-treated muscles. In conclusion, after isometric contractions, muscle cell membrane damage depends on Ca2+ influx and energy status and not on mechanical stress.
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Gong, Ming C., Sandrine Arbogast, Zhenheng Guo, Jeremy Mathenia, Wen Su, and Michael B. Reid. "Calcium-independent phospholipase A2 modulates cytosolic oxidant activity and contractile function in murine skeletal muscle cells." Journal of Applied Physiology 100, no. 2 (February 2006): 399–405. http://dx.doi.org/10.1152/japplphysiol.00873.2005.
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Phospholipase A2 (PLA2) activity supports production of reactive oxygen species (ROS) by mammalian cells. In skeletal muscle, endogenous ROS modulate the force of muscle contraction. We tested the hypothesis that skeletal muscle cells constitutively express the calcium-independent PLA2 (iPLA2) isoform and that iPLA2 modulates both cytosolic oxidant activity and contractile function. Experiments utilized differentiated C2C12 myotubes and a panel of striated muscles isolated from adult mice. Muscle preparations were processed for measurement of mRNA by real-time PCR, protein by immunoblot, cytosolic oxidant activity by the dichlorofluorescein oxidation assay, and contractile function by in vitro testing. We found that iPLA2 was constitutively expressed by all muscles tested (myotubes, diaphragm, soleus, extensor digitorum longus, gastrocnemius, heart) and that mRNA and protein levels were generally similar among muscles. Selective iPLA2 blockade by use of bromoenol lactone (10 μM) decreased cytosolic oxidant activity in myotubes and intact soleus muscle fibers. iPLA2 blockade also inhibited contractile function of unfatigued soleus muscles, shifting the force-frequency relationship rightward and depressing force production during acute fatigue. Each of these changes could be reproduced by selective depletion of superoxide anions using superoxide dismutase (1 kU/ml). These findings suggest that constitutively expressed iPLA2 modulates oxidant activity in skeletal muscle fibers by supporting ROS production, thereby influencing contractile properties and fatigue characteristics.
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Ponce-Hornos, J. E., E. A. Musi, and P. Bonazzola. "Role of extracellular calcium on heart muscle energetics: effects of verapamil." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 1 (January 1, 1990): H64—H72. http://dx.doi.org/10.1152/ajpheart.1990.258.1.h64.
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The mechanical and energetic effects of verapamil (VER) and reduction of extracellular Ca concentration ([Ca]o) were studied in the interventricular rabbit septa and the dog papillary muscle. Even though the negative inotropic effects of VER [i.e., decrease in developed tension (T), maximal rates of contraction (+T) and relaxation (-T), and tension time integral] qualitatively resemble [Ca]o reduction, VER also elicited an anti-relaxant effect (decrease in -T/T and prolongation of the last phase of relaxation) that was not found with [Ca]o reduction. Resting heat production was similar in both preparations and remained unaffected either by changes in [Ca]o or by the presence of VER. The ratio between T and active heat production per beat (H'a) under constant fiber length decreased with VER, and this decreased economy of contraction was more marked with the increase in contraction frequency. Conversely, the T/H'a remained unaltered with changes in [Ca]o. Tension-independent heat decreased in the presence of VER and, although muscle economy can be improved by increasing muscle length in a VER-treated muscle, it is not possible to achieve either the maximal T or the maximal contraction economy that can be obtained by stretching a nontreated muscle. It may be concluded that at constant fiber length and frequency of contraction VER decreases myocardial contractile force, impairs relaxation, and decreases contraction economy. Neither the mechanical nor the energetic effects of VER can be explained solely on the basis of a reduced extracellular Ca availability, so that either the density of the Ca that enters through the channel is different from that of other sources of Ca or VER has an effect on the cross-bridge cycling mechanism.
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Wong, Wai-Shiu, and Ralf G. Rahwan. "Pharmacological actions of the calcium antagonist propyl-methylenedioxyindene in skinned vascular smooth muscle." Canadian Journal of Physiology and Pharmacology 66, no. 8 (August 1, 1988): 1041–47. http://dx.doi.org/10.1139/y88-170.
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Previous studies provided strong evidence that propyl-methylenedioxyindene (pr-MDI) interfered with calcium at an intracellular site. To further characterize the mechanism of action of pr-MDI, its pharmacological actions on chemically skinned vascular smooth muscle were examined. Rat caudal artery strips were chemically skinned with saponin (0.15 mg/mL for 1 h). The efficiency of the skinning was evidenced by a loss of contractile response to 74 mM K+. The intactness of the regulatory and contractile proteins was ascertained by the ability of the skinned tissue to contract in response to Ca2+ (free Ca2+ concentration of 10−4 or 10−6 M). Caffeine (25 mM) induced contraction was used as an index of the functional integrity of the sarcoplasmic reticulum in the skinned preparations. Contraction of the skinned artery with a free Ca2+ concentration of 10−6 M was significantly obtunded by 1 × 10−4 M trifluoperazine (a calmodulin antagonist) but not by 1 × 10−4 M pr-MDI. Contraction of the skinned artery evoked by 25 mM caffeine in the absence of extracellular calcium was significantly obtunded by 1 × 10−4 M pr-MDI but not by 1 × 10−6 M nifedipine (a calcium channel blocker). The results indicate that pr-MDI acts intracellularly to block calcium mobilization from the sarcoplasmic reticulum without directly interfering with the regulatory and contractile proteins.
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Gerthoffer, William T. "Signal-Transduction Pathways that Regulate Visceral Smooth Muscle Function III. Coupling of muscarinic receptors to signaling kinases and effector proteins in gastrointestinal smooth muscles." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 5 (May 2005): G849—G853. http://dx.doi.org/10.1152/ajpgi.00530.2004.
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Stimulation of muscarinic M3 and M2 receptors on gastrointestinal smooth muscle elicits contraction via activation of G proteins that are coupled to a diverse set of downstream signaling pathways and effector proteins. Many studies suggest a canonical excitation-contraction coupling pathway that includes activation of phospholipases, production of inositol 1,4,5-trisphosphate and diacylglycerol, release of calcium from the sarcoplasmic reticulum, activation of L-type calcium channels, and activation of nonselective cation channels. These events lead to elevated intracellular calcium concentration, which activates myosin light chain kinase to phosphorylate and activate myosin II thus causing contraction. In addition, muscarinic receptors are coupled to signaling pathways that modulate the effect of activator calcium. The Rho/Rho kinase pathway inhibits myosin light chain phosphatase, one of the key steps in sensitization of the contractile proteins to calcium. Phosphatidylinositol 3-kinases and Src family tyrosine kinases are also activated by muscarinic agonists. Src family tyrosine kinases regulate L-type calcium and nonselective cation channels. Src activation also leads to activation of ERK and p38 MAPKs. ERK MAPKs phosphorylate caldesmon, an actin filament binding protein. P38 MAPKs activate phospholipases and MAPKAP kinase 2/3, which phosphorylate HSP27. HSP27 may regulate cross-bridge function, actin filament formation, and actin filament attachment to the cell membrane. In addition to the well-known role of M3 muscarinic receptors to regulate myoplasmic calcium levels, the integrated effect of muscarinic activation probably also includes signaling pathways that modulate phospholipases, cyclic nucleotides, contractile protein function, and cytoskeletal protein function.
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Wagner, Jamie, Erik Allman, Ashley Taylor, Kiri Ulmschneider, Timothy Kovanda, Bryne Ulmschneider, Keith Nehrke, and Maureen A. Peters. "A calcineurin homologous protein is required for sodium-proton exchange events in the C. elegans intestine." American Journal of Physiology-Cell Physiology 301, no. 6 (December 2011): C1389—C1403. http://dx.doi.org/10.1152/ajpcell.00139.2011.
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Caenorhabditis elegans defecation is a rhythmic behavior, composed of three sequential muscle contractions, with a 50-s periodicity. The motor program is driven by oscillatory calcium signaling in the intestine. Proton fluxes, which require sodium-proton exchangers at the apical and basolateral intestinal membranes, parallel the intestinal calcium flux. These proton shifts are critical for defecation-associated muscle contraction, nutrient uptake, and longevity. How sodium-proton exchangers are activated in time with intestinal calcium oscillation is not known. The posterior body defecation contraction mutant ( pbo-1) encodes a calcium-binding protein with homology to calcineurin homologous proteins, which are putative cofactors for mammalian sodium-proton exchangers. Loss of pbo-1 function results in a weakened defecation muscle contraction and a caloric restriction phenotype. Both of these phenotypes also arise from dysfunctions in pH regulation due to mutations in intestinal sodium-proton exchangers. Dynamic, in vivo imaging of intestinal proton flux in pbo-1 mutants using genetically encoded pH biosensors demonstrates that proton movements associated with these sodium-proton exchangers are significantly reduced. The basolateral acidification that signals the first defecation motor contraction is scant in the mutant compared with a normal animal. Luminal and cytoplasmic pH shifts are much reduced in the absence of PBO-1 compared with control animals. We conclude that pbo-1 is required for normal sodium-proton exchanger activity and may couple calcium and proton signaling events.