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Academic literature on the topic 'Calcium channels'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 July 2024

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Journal articles on the topic "Calcium channels"

1

Triggle, David J. "Calcium, calcium channels, and calcium channel antagonists." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1474–81. http://dx.doi.org/10.1139/y90-224.

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Voltage-dependent Ca2+ channels are an important pathway for Ca2+ influx in excitable cells. They also represent an important site of action for a therapeutic group of agents, the Ca2+ channel antagonists. These drugs enjoy considerable use in the cardiovascular area including angina, some arrhythmias, hypertension, and peripheral vascular disorders. The voltage-dependent Ca2+ channels exist in a number of subclasses characterized by electrophysiologic, permeation, and pharmacologic criteria. The Ca2+ channel antagonists, including verapamil, nifedipine, and diltiazem, serve to characterize the L channel class. This channel class has been characterized as a pharmacologic receptor, since it possesses specific drug-binding sites for both antagonists and activators and it is regulated by homologous and heterologous influences. The Ca2+ channels of both voltage- and ligand-regulated classes are likely to continue to be major research targets for new drug design and action.Key words: calcium, calcium channels, calcium antagonists, 1,4-dihydropyridines, channel regulation, receptor regulation.

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Greenberg, David A. "Calcium channels and calcium channel antagonists." Annals of Neurology 21, no. 4 (April 1987): 317–30. http://dx.doi.org/10.1002/ana.410210402.

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Collier, M. L., G. Ji, Y. X. Wang, and M. I. Kotlikoff. "Calcium-Induced Calcium Release in Smooth Muscle." Journal of General Physiology 115, no. 5 (May 1, 2000): 653–62. http://dx.doi.org/10.1085/jgp.115.5.653.

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Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L-type Ca2+ channels can open without triggering Ca2+ sparks and triggered Ca2+ sparks are often observed after channel closure. CICR is a function of the net flux of Ca2+ ions into the cytosol, rather than the single channel amplitude of L-type Ca2+ channels. Moreover, unlike CICR in striated muscle, calcium release is completely eliminated by cytosolic calcium buffering. Thus, L-type Ca2+ channels are loosely coupled to RYR through an increase in global [Ca2+] due to an increase in the effective distance between L-type Ca2+ channels and RYR, resulting in an uncoupling of the obligate relationship that exists in striated muscle between the action potential and calcium release.

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Mochida, Sumiko. "Presynaptic Calcium Channels." International Journal of Molecular Sciences 20, no. 9 (May 6, 2019): 2217. http://dx.doi.org/10.3390/ijms20092217.

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Presynaptic Ca2+ entry occurs through voltage-gated Ca2+ (CaV) channels which are activated by membrane depolarization. Depolarization accompanies neuronal firing and elevation of Ca2+ triggers neurotransmitter release from synaptic vesicles. For synchronization of efficient neurotransmitter release, synaptic vesicles are targeted by presynaptic Ca2+ channels forming a large signaling complex in the active zone. The presynaptic CaV2 channel gene family (comprising CaV2.1, CaV2.2, and CaV2.3 isoforms) encode the pore-forming α1 subunit. The cytoplasmic regions are responsible for channel modulation by interacting with regulatory proteins. This article overviews modulation of the activity of CaV2.1 and CaV2.2 channels in the control of synaptic strength and presynaptic plasticity.

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Gollasch, M., J. Hescheler, J. M. Quayle, J. B. Patlak, and M. T. Nelson. "Single calcium channel currents of arterial smooth muscle at physiological calcium concentrations." American Journal of Physiology-Cell Physiology 263, no. 5 (November 1, 1992): C948—C952. http://dx.doi.org/10.1152/ajpcell.1992.263.5.c948.

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Entry of Ca through voltage-dependent Ca channels is an important regulator of the function of smooth muscle, cardiac muscle, and neurons. Although Ca channels have been extensively studied since the first descriptions of Ca action potentials (P. Fatt and B. Katz. J. Physiol. Lond. 120: 171-204, 1953), the permeation rate of Ca through single Ca channels has not been measured directly under physiological conditions. Instead, single Ca channels have typically been examined using high concentrations (80-110 mM) of another divalent charge carrier, Ba, so as to maximize the amplitude of the single-channel currents. Calculations of unitary currents at 2 mM Ca indicated that the single-channel currents would be immeasurably small (i.e., < 0.1 pA). We provide here the first direct measurements of single Ca channel currents at a physiological Ca concentration. Contrary to earlier estimates, we have found that currents through single Ca channels in arterial smooth muscle are 0.1-0.3 pA at 2 mM Ca and physiological membrane potentials. These relatively large unitary currents permit direct measurement of Ca channel properties under conditions that do not distort their function. Our data also indicate that Ca permeates these channels at relatively high rates in physiological Ca concentrations and membrane potentials.

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Shuttleworth, T. J., and O. Mignen. "Calcium entry and the control of calcium oscillations." Biochemical Society Transactions 31, no. 5 (October 1, 2003): 916–19. http://dx.doi.org/10.1042/bst0310916.

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During oscillatory Ca2+ signals, the agonist-induced enhanced entry of extracellular Ca2+ plays a critical role in modulating the frequency of the oscillations. Although it was originally assumed that the entry of Ca2+ under these conditions occurred via the well-known, and apparently ubiquitous, store-operated mechanism, subsequent studies suggested that this was unlikely. It is now known that, in many cell types, a novel non-capacitative Ca2+-selective pathway whose activation is dependent on arachidonic acid is responsible, and the channels involved [ARC channels (arachidonate-regulated Ca2+ channels)] have been characterized. These ARC channels co-exist with the store-operated CRAC channels (Ca2+-release-activated Ca2+ channel) in cells, but each plays a unique and non-overlapping role in Ca2+ signalling. In particular, it is the ARC channels that are specifically activated at the low agonist concentrations that give rise to oscillatory Ca2+ signals and provide the predominant mode of Ca2+ entry under these conditions. The indications are that Ca2+ entry through the ARC channels increases the likelihood that low concentrations of Ins(1,4,5)P3 will trigger repetitive Ca2+ release. At higher agonist concentrations, store-depletion is more complete and sustained resulting in the activation of CRAC channels. At the same time the ARC channels are turned off, resulting in what we have described as a reciprocal regulation of these two distinct Ca2+ entry pathways.

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Triggle, C. R., and M. Wolowyk. "Calcium Channels Symposium." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1472–73. http://dx.doi.org/10.1139/y90-223.

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Calcium is an essential element for just about all cellular processes, and yet abnormally high levels of cellular calcium can cause cell death. The processes that control cellular levels of this metal ion are thus of critical importance to both normal and pathophysiological conditions. Essential in the regulation of intracellular calcium levels are the calcium channels associated with cell membranes, for instance, with the plasma and sarcoplasmic reticulum membranes of muscle cells. In recent years, there has been a tremendous increase in our knowledge of the structure and function of these channels. However, we also now realize that the term "calcium channels" is used to refer to a rather heterogeneous population of entities. In some instances, notably receptor-operated calcium channels, we have only indirect evidence for their existence, whereas with the voltage-dependent channels, considerable information is now available on their comparative physiology, pharmacology, and biochemistry. The main objective of the Symposium presented in Calgary during the 1989 CFBS meeting was to bring together experts in the area of the calcium channels associated with both smooth and striated muscle function so that they could present the current state of knowledge in this area.Dr. David Triggle, from the State University of New York in Buffalo, reviewed the importance of calcium and calcium channels in cellular function and highlighted the pharmacology of calcium channel antagonists particularly with respect to their effects on the L-type calcium channels associated with smooth muscle. Dr. Sidney Fleischer from Vanderbilt University, Nashville, Tennessee, focused on his work associated with the isolation and characterization of the calcium release channel – ryanodine receptor of the sarcoplasmic reticulum from striated muscle. Dr. Fleischer has referred interested readers to his recent review in the 1989 issue of the Annual Reviews of Biophysics and Biophysical Chemistry (18: 333–364). Dr. Balwant Tuana from the University of Ottawa presented an update complemented by original data from his laboratory in the Department of Pharmacology on the current state of knowledge of the structure of the L-type calcium channel associated with both skeletal and cardiac muscle. The last two speakers, Dr. Wayne Giles and Dr. Hamid Akbarali, both from the Department of Medical Physiology at the University of Calgary, completed the program by presenting a review of data concerning the electrical physiological properties of calcium-activated channels in cardiac and smooth muscle. Their manuscript highlights their recent studies, with co-workers in Calgary, of the properties of calcium-activated potassium currents from the human cystic artery.The organizers of this symposium, hosted by the Pharmacological Society of Canada, gratefully acknowledge the financial support of the Alberta Heart and Stroke Foundation, Alberta Heritage Foundation for Medical Research, Canadian Heart and Stroke Foundation, Canadian Federation of Biological Societies, Charles River Laboratories (Canada Ltd.), SynPhar Laboratories Inc., Fisher Scientific Ltd., Novopharm Ltd., and Mandel Scientific Co. Ltd. The artistic contribution from Sylvia Ficken of Medical Audiovisual Services in the Faculty of Medicine at Memorial University of Newfoundland, who drew the symposium logo reproduced on the title page, is also gratefully acknowledged.

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Friedman, P. A., and F. A. Gesek. "Hormone-responsive Ca2+ entry in distal convoluted tubules." Journal of the American Society of Nephrology 4, no. 7 (January 1994): 1396–404. http://dx.doi.org/10.1681/asn.v471396.

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This editorial review focuses on recent observations regarding the mechanism and regulation of calcium transport in hormone-sensitive distal convoluted tubules. Parathyroid hormone (PTH) and calcitonin increase active calcium absorption by distal convoluted tubules. Occupancy of these peptide hormone receptors results in the activation of both protein kinase A and protein kinase C. The inhibition of either kinase blocks calcium transport. The time course of stimulation of calcium entry in distal convoluted tubules by PTH is slow compared with that by calcitonin. The latency associated with PTH action may be due to the induction of protein synthesis. PTH and calcitonin hyperpolarize membrane voltage, which in turn increases calcium entry. Calcium entry is mediated by calcium channels. These channels exhibit a low, single-channel conductance and are sensitive to dihydropyridine-type calcium channel blockers. Unlike L-type calcium channels, the channel open probability of distal convoluted tubule calcium entry channels is increased upon hyperpolarization. This novel combination of properties suggests that the underlying structure of these calcium entry channels may be unique.

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Reuter, H., S. Kokubun, and B. Prod'hom. "Properties and modulation of cardiac calcium channels." Journal of Experimental Biology 124, no. 1 (September 1, 1986): 191–201. http://dx.doi.org/10.1242/jeb.124.1.191.

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Voltage-dependent calcium channels are widely distributed in excitable membranes and are involved in the regulation of many cellular functions. These channels can be modulated by neurotransmitters and drugs. There is one particular type of calcium channel in cardiac cells (L-type) whose gating is affected in different ways by beta-adrenoceptor and 1,4-dihydropyridine agonists. We have analysed single calcium channel currents (i) in myocytes from rat hearts in the absence and presence of isoproterenol or 8-bromo-cAMP. We have found that both compounds have similar effects on calcium channel properties. They increase the overall open state probability (po) of individual calcium channels while i remains unaffected. Analysis of the gating kinetics of calcium channels showed: a slight increase in the mean open times of calcium channels, a reduction in time intervals between bursts of channel openings, an increase in burst length and a prominent reduction in failures of calcium channels to open upon depolarization. These kinetic changes caused by isoproterenol and 8-bromo-cAMP can account for the increase in po. Since the macroscopic calcium current, ICa, can be described by ICa = N X po X i, the increase in po accounts for the well-known increase in ICa by beta-adrenergic catecholamines. Cyclic AMP-dependent phosphorylation of calcium channels is a likely metabolic step involved in this modulation. Another class of drug that modulates calcium channel gating is the 1,4-dihydropyridines which can either enhance or reduce ICa, either by prolonging the open state of the channels or by facilitating the inactivated state. Both effects depend strongly on membrane potential and are independent of cyclic AMP-dependent phosphorylation reactions.

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Kolesnikov, D. O., E. R. Grigorieva, M. A. Nomerovskaya, D. S. Reshetin, A. V. Shalygin, and E. V. Kaznacheyeva. "The Effect of Calcium Ions on the Electrophysiological Properties of Single ANO6 Channels." Acta Naturae 16, no. 1 (May 10, 2024): 40–47. http://dx.doi.org/10.32607/actanaturae.27338.

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Proteins belonging to the anoctamin (ANO) family form calcium-activated chloride channels (CaCCs). The most unusual member of this family, ANO6 (TMEM16F), simultaneously exhibits the functions of calcium-dependent scramblase and the ion channel. ANO6 affects the plasma membrane dynamics and phosphatidylserine transport; it is also involved in programmed cell death. The properties of ANO6 channels remain the subject of debate. In this study, we investigated the effect of variations in the intracellular and extracellular concentrations of calcium ions on the electrophysiological properties of endogenous ANO6 channels by recording single ANO6 channels. It has been demonstrated that (1) a high calcium concentration in an extracellular solution increases the activity of endogenous ANO6 channels, (2) the permeability of endogenous ANO6 channels for chloride ions is independent of the extracellular concentration of calcium ions, (3) that an increase in the intracellular calcium concentration leads to the activation of endogenous ANO6 channels with double amplitude, and (4) that the kinetics of the channel depend on the plasma membrane potential rather than the intracellular concentration of calcium ions. Our findings give grounds for proposing new mechanisms for the regulation of the ANO6 channel activity by calcium ions both at the inner and outer sides of the membrane.

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Dissertations / Theses on the topic "Calcium channels"

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Roberts, Dewi. "Calcium-dependent inactivation of Cav1.3 calcium channels." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446186.

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Peterson, Blaise. "Molecular determinants of dihydropyridine binding on L-type calcium channels /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6269.

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Farrington, Jasmine. "Calcium release activated calcium channels in human lung mast cells." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6609/.

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Nakayama, Shinsuke. "Calcium channels in detrusor smooth muscle." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334328.

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Xie, Mian. "Calcium Channel Beta Subunits and SCA6-Type Calcium Channel Alpha Subunits C-Termini Regulate Targeting and Function of Presynaptic Calcium Channels in Hippocampal Neurons." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1188326628.

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Yasuda, Takahiro. "Modulation of calcium channel function and toxin sensitivity by auxiliary subunits /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18052.pdf.

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Doughty, Stephen William. "Molecular modelling of voltage-gated calcium channels." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362014.

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Warburton, Steven Peter Marc. "Calcium ion channels in insect skeletal muscle." Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363592.

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Richardson, C. Mark. "Presynaptic calcium channels in skate electric organ." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319614.

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Pearson, Hugh Anthony. "Physiology and pharmacology of insect calcium channels." Thesis, University College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308295.

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Books on the topic "Calcium channels"

1

A, Allen T. Jeff, Noble D, and Reuter Harald, eds. Sodium-calcium exchange. Oxford: Oxford University Press, 1989.

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1921-, Hurwitz Leon, Partridge L. Donald, and Leach John K, eds. Calcium channels: Their properties, functions, regulation, and clinical relevance. Boca Raton, Fla: CRC Press, 1991.

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Weiss, Norbert, and Alexandra Koschak, eds. Pathologies of Calcium Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40282-1.

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Zamponi, Gerald Werner, and Norbert Weiss, eds. Voltage-Gated Calcium Channels. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08881-0.

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Zamponi, Gerald W. Voltage-gated calcium channels. New York: Springer, 2011.

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1936-, Grinnell Alan D., Armstrong David 1951-, Jackson Meyer B, and Eckert Roger, eds. Calcium and ionchannel modulation. New York: Plenum, 1988.

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I, McDonough Stefan, ed. Calcium channel pharmacology. New York: Kluwer Academic/Plenum Publishers, 2004.

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Stephens, Gary, and Sumiko Mochida, eds. Modulation of Presynaptic Calcium Channels. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6334-0.

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Dennis, W. Wray, Norman Robert I, Hess Peter 1951-, and New York Academy of Sciences., eds. Calcium channels: Structure and function. New York, N.Y: New York Academy of Sciences, 1989.

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W, Putney James, ed. Calcium signaling. Boca Raton, Fla: CRC Press, 2000.

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Book chapters on the topic "Calcium channels"

1

Ertel, Eric, and Théophile Godfraind. "Calcium channel blockers and calcium channels." In Calcium Channel Blockers, 11–80. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7859-3_2.

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Ducsay, Charles A. "Calcium Channels." In Uterine Function, 169–94. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0575-0_6.

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Nelson, Mark T. "Calcium Channels." In Ion Channel Reconstitution, 507–22. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-1361-9_20.

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Leslie, Steven W. "Calcium Channels." In Recent Developments in Alcoholism, 289–302. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-1684-6_10.

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Reynolds, Ian J., and Solomon H. Snyder. "Calcium Antagonist Receptors." In Ion Channels, 213–49. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-7302-9_6.

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Turner, Ray W. "Cav3 Calcium Channel Interactions with Potassium Channels." In Voltage-Gated Calcium Channels, 237–52. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08881-0_10.

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Bangalore, R., J. Ferrante, M. Hawthorn, W. Zheng, A. Rutledge, M. Gopalakrishnan, and D. J. Triggle. "The Regulation of Neuronal Calcium Channels." In Calcium Antagonists, 221–29. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1725-8_31.

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Beech, D. J., and T. B. Bolton. "Calcium Channels in Intestinal Smooth Muscle." In Calcium Antagonists, 285–90. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1725-8_39.

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Pietrobon, Daniela. "Cav2.1 Channels and Migraine." In Pathologies of Calcium Channels, 3–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_1.

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Wissenbach, Ulrich. "Pharmacology of TRPV Channels." In Pathologies of Calcium Channels, 549–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_27.

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Conference papers on the topic "Calcium channels"

1

Jenson, Lacey J. "Voltage- and calcium-activated chloride channels in insect physiological systems." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93221.

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Pe�aranda, Angelina, Blas Echebarria, Enrique Alvarez-Lacalle, and Inmaculada R. Cantalapiedra. "Effects of Small Conductance Calcium Activated Potassium Channels in Cardiac Myocytes." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.308-050.

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Kaufman, I., R. Tindjong, D. G. Luchinsky, P. V. E. McClintock, and R. S. Eisenberg. "Resonant multi-ion conduction in a simple model of calcium channels." In 2013 International Conference on Noise and Fluctuations (ICNF). IEEE, 2013. http://dx.doi.org/10.1109/icnf.2013.6578926.

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Yu-Hong, Zhang, Zhan Yong, Zhao Tong-Jun, Han Ying-Rong, and Liu Hui. "Mechanism of Permeation in Calcium Channels Activation by Applied Magnetic Fields." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352558.

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Cheng, Pan, Wanyi Tang, and Hao He. "Two-photon activation of endogenous store-operated calcium channels without optogenetics." In Multiphoton Microscopy in the Biomedical Sciences XVIII, edited by Ammasi Periasamy, Peter T. So, Xiaoliang S. Xie, and Karsten König. SPIE, 2018. http://dx.doi.org/10.1117/12.2286586.

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Neamtu, Bogdan Mihai, Alexandru Farcuta, Beatrice Mihaela Radu, Andrei Dragomir, Ionela Maniu, and Daniel Dumitru Banciu. "Low Level Laser Modulation of Calcium Channels Leads to Neuronal Extensions Growth." In 2019 E-Health and Bioengineering Conference (EHB). IEEE, 2019. http://dx.doi.org/10.1109/ehb47216.2019.8969900.

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Dias, Thales Augusto Oliveira, and Silvia Graciela Ruginsk Leitão. "Participation of calcium channels in the action of angiotensin II in astrocytes." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.299.

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Background: The renin-angiotensin-aldosterone system is the main regulator of blood pressure and blood volume, with most effects being mediated by angiotensin II (Ang-II) - responsible, in the central nervous system, for actions such as thirst and sodium appetite. Astrocytes are believed to mediate such a response, as they express receptors for Ang-II and respond directly to dehydration with impacting morphological changes in the synaptic microenvironment. Many of its functions involve L-type calcium channels (LTCCs). Objectives: Evaluate the participation of LTCCs in the effects induced by AngII in cultured hypothalamic astrocytes. Methods: The effect of incubation with verapamil on the morphological responses induced by Ang-II was evaluated in hypothalamic astrocyte culture, by analyzing the expression of the cytoskeletal protein GFAP and the cell viability by the MTT assay, by immunofluorescence. Results: Incubation with Ang-II reduced the cell area considerably due to GFAP expression in relation to the control group (DMEM p<0.001), indicating that the results observed on GFAP expression did not result from cell death. Conclusion: Incubation with Ang-II alters the astrocyte morphology, reducing its area, effect at least in part, blocked by the action of Verapamil, indicating the participation of LTCCs in the mediation of this process.

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Trippa, Giuliana, and Roshan J. J. Jachuck. "Characterization of Mixing Efficiency in Narrow Channels by Using the Iodide-Iodate Reaction System." In ASME 2004 2nd International Conference on Microchannels and Minichannels. ASMEDC, 2004. http://dx.doi.org/10.1115/icmm2004-2413.

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Microreactors and narrow channel reactors have found an increasing number of applications in the last few years for their enhanced heat and mass transfer properties if compared to traditional process equipment. In this investigation, mixing efficiency in a narrow channel reactor system has been studied by using the iodide-iodate scheme of parallel competing reactions that leads to the formation of iodine. The tested system is constituted by two reactors machined in Perspex. The two channels have identical configuration and a square cross section with diagonal lines of 1·10−3 m and 2·10−3 m respectively. Influence of flow rate on the selectivity towards iodine has been studied for both reactors. This allows the characterization of mixing intensity at varying operating conditions. The results obtained reflect the expected influence of flow rate and channel characteristic dimension on mixing efficiency. This investigation has been carried out on the same reactor system that had been previously used for studying the precipitation of calcium carbonate from solutions of sodium carbonate and calcium nitrate. In fact, a study on mixing efficiency is particularly useful in the case of precipitation reactions as poor mixing can lead to a final product that does not respect marketing requirements in terms of particle size and particle size distribution. The information acquired in the two investigations can constitute the basis for the design of modules based on narrow channel technology for the production of powders and slurries with controlled properties.

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Rink, T. J. "CALCIUM IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644772.

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Studies with calcium ionophores, permeabilised platelets, and platelets containing fluorescent calcium indicators quin2 and fura-2 have shown that elevation [Ca2+]i is an effective trigger for shape-change, aggregation, secretion and release of TxA2; and that elevation of [Ca2+]i is an important part of a complex “activation cascade” set up by natural agonists combining with their surface receptors. We have used calcium ionophores to impose [Ca2+]i changes, monitored by indicator dyes, to construct [Ca2+]i/function relationships for shape-change, secretion, aggregation, arachidonic acid release, TxA2 production, and myosin phosphorylation in intact platelets(e.g.1,2). Some of these functions can also be studied by analagous experiments using Ca2+-buffers to set known [Ca2+]i in permeabilised platelets. Our ability to monitor and modulate [Ca2+]i with fluorescent indicators has also allowed us to see what happens when [Ca2+]i changes are greately reduced or even absent and to investigate other pathways of intracellular activation. We think that formation of diacyl glycerol and activation of protein kinase-C can explain, some, but not all, of the cell activation that some agonists can apparently evoke at or near resting [Ca2+]i, and that combined or synergistic actions of Ca2+ and other intracellular mediators is the usual basis for physiological activation(3). Most agonists seem to promote both Ca2+ entry across the plasma membrahe and discharge from intracellular organelles, presumably the dense tubular system. The available evidence fits with the prevailing idea that Ins 1,4,5 P3 formed by agonist evoked hydrolysis of PIP2, is the internal messenger for Ca2+ release. Our kinetic measurements of [Ca2+]i transients require that optimal concentrations of InsP3 are formed within 250 milliseconds(4,5). The question of whether ADP receptors in human platelets are directly coupled with PIP2 breakdown remains contentious. Probably they do, weakly, and the differences from most other receptors are quantitative rather than qualitative. We do not understand the mechanisms of agonist-evoked Ca2+-entry; there is now plenty of evidence that argues against a role for membrane depolarisation and voltage-gated Ca channels, including some recent work with ionic substitution(5). Stopped-flow fluorescence analysis of [Ca2+]i rises in fura-2-loaded human platelets reveals some intriguing new insights(4,5). With thrombin, vasopressin and PAF at optimal concentrations, there is a highly reproducible delay before the signal starts to rise, which is approximately 250msec in the absence of external calcium compared to 190msec in the presence of external calcium. This suggests that Ca entry leads internal release, and gives ample time for complex coupling mechanisms for both processes.The delay with ADP, in the presence of external calcium, is much smaller suggesting a different coupling mechanism for Ca entry.

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Kovalenko, S. G., S. R. Frolova, and K. I. Agladze. "COMPARISON OF THE EFFECTS OF CARDIOPLEGIC SOLUTIONS NORMACOR AND CUSTODIOL ON THE RESTORATION OF ELECTROPHYSIOLOGICAL ACTIVITY OF HUMAN CARDIOMYOCYTES FOLLOWING CARDIAC SURGERY." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-182.

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The study focuses on investigating the restoration of voltage-gated ion channels in human cardiomyocytes after cardiac surgery. A protocol for isolating mature cardiomyocytes from biopsy samples was optimized, and the restoration pattern of L-type calcium channels, fast sodium channels and slow potassium channels following surgeries using cardioplegic solutions Custodiol and Normacor was identified.

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Reports on the topic "Calcium channels"

1

Sze, Heven. Identifying Calcium Channels and Porters in Plant Membranes. Office of Scientific and Technical Information (OSTI), April 1998. http://dx.doi.org/10.2172/7215.

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2

Schroeder, Julian I. Physiology and Regulation of Calcium Channels in Stomatal Guard Cells. Office of Scientific and Technical Information (OSTI), May 2007. http://dx.doi.org/10.2172/887459.

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Philosoph-Hadas, Sonia, Richard Crain, Shimon Meir, Nehemia Aharoni, and Susan Lurie. Calcium-Mediated Signal Transduction during Leaf Senescence. United States Department of Agriculture, November 1995. http://dx.doi.org/10.32747/1995.7604925.bard.

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We have examined the possibility that modulation of [Ca2+]cyt may represent a signal which induces senescence processes in leaves, through triggering of lipid hydrolysis leading to the cascade of detriorative events. Characterization of the signal transduction components operating during leaf senescence was gained by studying various Ca2+-dependent activities of parsley and chrysanthemum leaves, in relation to several senescence functions, and in response to senescence-modulating hormones (ethylene,ABA, BA and IAA). Some innovative findings regarding the control of senescence processes by [Ca2+]cyt were established: Several Ca2+-or CaM-related compounds were shown to modulate [Ca2+]cyt and action, thereby affecting whole leaf senescence. The involvement of [Ca2+]cyt in mediating the effects of senescence-modulating hormones has been demonstrated. Loss of energized Ca2+-transport capability of PM was found to an early event in leaf senescence, which occurs before changes in senescence parameters are observed, and while other PM ATPase enzymes still retain about 50% of their activities. A general pattern of increased phosphorylation of PM proteins with advanced senescence, which could be modified by plant hormones applied in vivo (BA) or in vitro (ABA), sa found. Taken together, all this indirect evidence indicate that [Ca2+]cyt is elevated due to the senescence-induced decrease in the ability to extrude Ca2+, which results particularly from reduced PM Ca2++-transport capability rather than increased operation of Ca2+ channels or elevated Ins(1,4,5)P3 levels. The direct proof for such a senescence-related elevation in [Ca2+]cyt was provided for the first time by the Ca2+ imaging measures with fura-2, showing a rise in [Ca2+]cyt of mesophyll cells upon senescence induction, which preceeded changes in typical senescence characteristics. This research provides strong evidence for regarding the rise in [Ca2+]cyt as a primary event in induction of the senescence syndrome in detached leaves. The findings have also broad implications for postharvest handling of leafy crops and ornamentals, and open new avenues for employing Ca2+-related inhibitors to delay leaf senescence.

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Freeman, Michael R. The Calcium Channel CaT1 in Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada443349.

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Owen, Laura. Modulation of the Cardiac Calcium Release Channel by Homocysteine Thiolactone. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2070.

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Karen S. Schumaker. Molecular Characterization of the Role of a Calcium Channel in Plant Development. Office of Scientific and Technical Information (OSTI), December 2004. http://dx.doi.org/10.2172/835288.

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7

Dornan, Thomas. Calcium Transport Inhibition, Stimulation, and Light Dependent Modulation of the Skeletal Calcium Release Channel (RyR1) by the Prototropic Forms of Pelargonidin. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1930.

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Yalovsky, Shaul, and Julian Schroeder. The function of protein farnesylation in early events of ABA signal transduction in stomatal guard cells of Arabidopsis. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7695873.bard.

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Loss of function mutations in the farnesyltransferase β subunit gene ERA1 (enhanced response to abscisic acid), cause abscisic acid hypersensitivity in seedlings and in guard cells. This results in slowed water loss of plants in response to drought. Farnesyltransferase (PFT) catalyses the attachment of the 15-carbon isoprenoid farnesyl to conserved cysteine residues located in a conserved C-terminal domain designated CaaX box. PFT is a heterodimeric protein comprised of an a and b sununits. The a subunit is shared between PFT and geranylgeranyltransferase-I (PGGTI) which catalyses the attachemt of the 20-carbon isoprenoid geranylgeranyl to CaaX box proteins in which the last amino acid is almost always leucine and in addition have a polybasic domain proximal to the CaaL box. Preliminary data presented in the proposal showed that increased cytoplasmic Ca2+ concentration in stomal guard cells in response to non-inductive ABA treatements. The goals set in the proposal were to characterize better how PFT (ERA1) affects ABA induced Ca2+ concentrations in guard cells and to identify putative CaaX box proteins which function as negative regulators of ABA signaling and which function is compromised in era1 mutant plants. To achieve these goals we proposed to use camelion Ca2+ sensor protein, high throughput genomic to identify the guard cell transcriptome and test prenylation of candidate proteins. We also proposed to focus our efforts of RAC small GTPases which are prenylated proteins which function in signaling. Our results show that farnesyltransferaseprenylates protein/s that act between the points of ABA perception and the activation of plasma membrane calcium influx channels. A RAC protein designated AtRAC8/AtRop10 also acts in negative regulation of ABA signaling. However, we discovered that this protein is palmitoylated and not prenylated although it contains a C-terminal CXXX motif. We further discovered a unique C-terminal sequence motif required for membrane targeting of palmitoylatedRACs and showed that their function is prenylation independent. A GC/MS based method for expression in plants, purification and analysis of prenyl group was developed. This method would allow highly reliable identification of prenylated protein. Mutants in the shared α subunit of PFT and PGGT-I was identified and characterized and was shown to be ABA hypersensitive but less than era1. This suggested that PFT and PGGT-I have opposing functions in ABA signaling. Our results enhanced the understanding of the role of protein prenylation in ABA signaling and drought resistance in plants with the implications of developing drought resistant plants. The results of our studies were published 4 papers which acknowledge support from BARD.

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Fukuta, Hidekatsu, Toshihiko Goto, and Takeshi Kamiya. Effects of calcium channel blockers in patients with heart failure with preserved ejection fraction: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2024. http://dx.doi.org/10.37766/inplasy2024.3.0097.

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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.

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