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Journal articles on the topic 'Sodium calcium exchange'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Schoenmakers, T. J., and G. Flik. "Sodium-extruding and calcium-extruding sodium/calcium exchangers display similar calcium affinities." Journal of Experimental Biology 168, no. 1 (July 1, 1992): 151–59. http://dx.doi.org/10.1242/jeb.168.1.151.

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Na+/Ca2+ exchange activities in purely inside-out and mixed inside-out and right-side-out fish enterocyte basolateral plasma membrane vesicle preparations display equal affinities for Ca2+, showing that only the intracellular Ca2+ transport site of the Na+/Ca2+ exchanger is detected in experiments on vesicle preparations with mixed orientation. Therefore, Ca2+ pump and Na+/Ca2+ exchange activity may be compared directly without correction for vesicle orientation. The Na+/Ca2+ exchange activity in fish enterocyte vesicles is compared to the activity found in dog erythrocyte vesicles. The calcium-extruding exchanger in fish basolateral plasma membranes shows values of Km and V(max) for calcium similar to those found for the sodium-extruding exchanger in dog erythrocyte membranes, indicating that differences in electrochemical gradients underlie the difference in cellular function of the two exchangers.

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2

Johnson, E., and R. Lemieux. "Sodium-calcium exchange." Science 251, no. 4999 (March 15, 1991): 1370. http://dx.doi.org/10.1126/science.1848371.

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3

Goldhaber, Joshua I. "Sodium-Calcium Exchange." Circulation Research 85, no. 11 (November 26, 1999): 982–84. http://dx.doi.org/10.1161/01.res.85.11.982.

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4

Schnetkamp, Paul. "Sodium-Calcium Exchange." Trends in Neurosciences 13, no. 9 (September 1990): 385. http://dx.doi.org/10.1016/0166-2236(90)90024-5.

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5

Philipson, Kenneth D., and Debora A. Nicoll. "Sodium-calcium exchange." Current Opinion in Cell Biology 4, no. 4 (August 1992): 678–83. http://dx.doi.org/10.1016/0955-0674(92)90089-u.

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6

HALE, CALVIN C., JULIE BOSSUYT, CHANANADA K. HILL, ELMER M. PRICE, DAN H. SCHULZE, JON W. LEDERER, ROBERTO POLJAK, and BRADFORD C. BRADEN. "Sodium-Calcium Exchange Crystallization." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 100–102. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04725.x.

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7

KANG, TONG MOOK, MARK STECIUK, and DONALD WILLIAM HILGEMANN. "Sodium-Calcium Exchange Stoichiometry." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 142–51. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04733.x.

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8

Reeves, John P., and Madalina Condrescu. "Allosteric Activation of Sodium–Calcium Exchange Activity by Calcium." Journal of General Physiology 122, no. 5 (October 27, 2003): 621–39. http://dx.doi.org/10.1085/jgp.200308915.

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The activity of the cardiac Na+/Ca2+ exchanger is stimulated allosterically by Ca2+, but estimates of the half-maximal activating concentration have varied over a wide range. In Chinese hamster ovary cells expressing the cardiac Na+/Ca2+ exchanger, the time course of exchange-mediated Ca2+ influx showed a pronounced lag period followed by an acceleration of Ca2+ uptake. Lag periods were absent in cells expressing an exchanger mutant that was not dependent on regulatory Ca2+ activation. We assumed that the rate of Ca2+ uptake during the acceleration phase reflected the degree of allosteric activation of the exchanger and determined the value of cytosolic Ca2+ ([Ca2+]i) at which the rate of Ca2+ influx was half-maximal (Kh). After correcting for the effects of mitochondrial Ca2+ uptake and fura-2 buffering, Kh values of ∼300 nM were obtained. After an increase in [Ca2+]i, the activated state of the exchanger persisted following a subsequent reduction in [Ca2+]i to values <100 nM. Thus, within 30 s after termination of a transient increase in [Ca2+]i, exchange-mediated Ca2+ entry began without a lag period and displayed a linear rate of Ca2+ uptake in most cells; a sigmoidal time course of Ca2+ uptake returned 60–90 s after the transient increase in [Ca2+]i was terminated. Relaxation of the activated state was accelerated by the activity of the endoplasmic reticulum Ca2+ pump, suggesting that local Ca2+ gradients contribute to maintaining exchanger activation after the return of global [Ca2+]i to low values.

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9

Blaustein, Mordecai P., and W. Jonathan Lederer. "Sodium/Calcium Exchange: Its Physiological Implications." Physiological Reviews 79, no. 3 (July 1, 1999): 763–854. http://dx.doi.org/10.1152/physrev.1999.79.3.763.

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The Na+/Ca2+exchanger, an ion transport protein, is expressed in the plasma membrane (PM) of virtually all animal cells. It extrudes Ca2+in parallel with the PM ATP-driven Ca2+pump. As a reversible transporter, it also mediates Ca2+entry in parallel with various ion channels. The energy for net Ca2+transport by the Na+/Ca2+exchanger and its direction depend on the Na+, Ca2+, and K+gradients across the PM, the membrane potential, and the transport stoichiometry. In most cells, three Na+are exchanged for one Ca2+. In vertebrate photoreceptors, some neurons, and certain other cells, K+is transported in the same direction as Ca2+, with a coupling ratio of four Na+to one Ca2+plus one K+. The exchanger kinetics are affected by nontransported Ca2+, Na+, protons, ATP, and diverse other modulators. Five genes that code for the exchangers have been identified in mammals: three in the Na+/Ca2+exchanger family ( NCX1, NCX2, and NCX3) and two in the Na+/Ca2+plus K+family ( NCKX1 and NCKX2). Genes homologous to NCX1 have been identified in frog, squid, lobster, and Drosophila. In mammals, alternatively spliced variants of NCX1 have been identified; dominant expression of these variants is cell type specific, which suggests that the variations are involved in targeting and/or functional differences. In cardiac myocytes, and probably other cell types, the exchanger serves a housekeeping role by maintaining a low intracellular Ca2+concentration; its possible role in cardiac excitation-contraction coupling is controversial. Cellular increases in Na+concentration lead to increases in Ca2+concentration mediated by the Na+/Ca2+exchanger; this is important in the therapeutic action of cardiotonic steroids like digitalis. Similarly, alterations of Na+and Ca2+apparently modulate basolateral K+conductance in some epithelia, signaling in some special sense organs (e.g., photoreceptors and olfactory receptors) and Ca2+-dependent secretion in neurons and in many secretory cells. The juxtaposition of PM and sarco(endo)plasmic reticulum membranes may permit the PM Na+/Ca2+exchanger to regulate sarco(endo)plasmic reticulum Ca2+stores and influence cellular Ca2+signaling.

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10

Philipson, Kenneth D. "Cardiac sodium-calcium exchange research." Trends in Cardiovascular Medicine 2, no. 1 (January 1992): 12–14. http://dx.doi.org/10.1016/1050-1738(92)90038-t.

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11

Ravens, Ursula, and Erich Wettwer. "Modulation of Sodium/Calcium Exchange." Journal of Cardiovascular Pharmacology 14, Supplement 3 (1989): S30—S35. http://dx.doi.org/10.1097/00005344-198914003-00007.

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12

Hryshko, L. V., and K. D. Philipson. "Sodium-calcium exchange: Recent advances." Basic Research in Cardiology 92, S1 (1997): 45–51. http://dx.doi.org/10.1007/bf00794067.

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13

Hilgemann, D. W., S. Matsuoka, G. A. Nagel, and A. Collins. "Steady-state and dynamic properties of cardiac sodium-calcium exchange. Sodium-dependent inactivation." Journal of General Physiology 100, no. 6 (December 1, 1992): 905–32. http://dx.doi.org/10.1085/jgp.100.6.905.

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Sodium-calcium exchange current was isolated in inside-out patches excised from guinea pig ventricular cells using the giant patch method. The outward exchange current decayed exponentially upon activation by cytoplasmic sodium (sodium-dependent inactivation). The kinetics and mechanism of the inactivation were studied. (a) The rate of inactivation and the peak current amplitude were both strongly temperature dependent (Q10 = 2.2). (b) An increase in cytoplasmic pH from 6.8 to 7.8 attenuated the current decay and shifted the apparent dissociation constant (Kd) of cytoplasmic calcium for secondary activation of the exchange current from 9.6 microM to < 0.3 microM. (c) The amplitude of exchange current decreased synchronously over the membrane potential range from -120 to 60 mV during the inactivation, indicating that voltage dependence of the exchanger did not change during the inactivation process. The voltage dependence of exchange current also did not change during secondary modulation by cytoplasmic calcium and activation by chymotrypsin. (d) In the presence of 150 mM extracellular sodium and 2 mM extracellular calcium, outward exchange current decayed similarly upon application of cytoplasmic sodium. Upon removal of cytoplasmic sodium in the presence of 2-5 microM cytoplasmic free calcium, the inward exchange current developed in two phases, a fast phase within the time course of solution changes, and a slow phase (tau approximately 4 s) indicative of recovery from sodium-dependent inactivation. (e) Under zero-trans conditions, the inward current was fully activated within solution switch times upon application of cytoplasmic calcium and did not decay. (f) The slow recovery phase of inward current upon removal of cytoplasmic sodium was also present under the zero-trans condition. (g) Sodium-dependent inactivation shows little or no dependence on membrane potential in guinea pig myocyte sarcolemma. (h) Sodium-dependent inactivation of outward current is attenuated in rate and extent as extracellular calcium is decreased. (i) Kinetics of the sodium-dependent inactivation and its dependence on major experimental variables are well described by a simple two-state inactivation model assuming one fully active and one fully inactive exchanger state, whereby the transition to the inactive state takes place from a fully sodium-loaded exchanger conformation with cytoplasmic orientation of binding sites (E1.3Ni).

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14

Alexander, R. Todd, Henrik Dimke, and Emmanuelle Cordat. "Proximal tubular NHEs: sodium, protons and calcium?" American Journal of Physiology-Renal Physiology 305, no. 3 (August 1, 2013): F229—F236. http://dx.doi.org/10.1152/ajprenal.00065.2013.

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Na+/H+ exchange activity in the apical membrane of the proximal tubule is fundamental to the reabsorption of Na+ and water from the filtrate. The role of this exchange process in bicarbonate reclamation and, consequently, the maintenance of acid-base homeostasis has been appreciated for at least half a century and remains a pillar of renal tubular physiology. More recently, apical Na+/H+ exchange, mediated by Na+/H+ exchanger isoform 3 (NHE3), has been implicated in proximal tubular reabsorption of Ca2+ and Ca2+ homeostasis in general. Overexpression of NHE3 increased paracellular Ca2+ flux in a proximal tubular cell model. Consistent with this observation, mice with genetic deletion of Nhe3 have a noticable renal Ca2+ leak. These mice also display decreased intestinal Ca2+ uptake and osteopenia. This review highlights the traditional roles of proximal tubular Na+/H+ exchange and summarizes recent novel findings implicating the predominant isoform, NHE3, in Ca2+ homeostasis.

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15

Hilgemann, Donald W. "Numerical approximations of sodium-calcium exchange." Progress in Biophysics and Molecular Biology 51, no. 1 (January 1988): 1–45. http://dx.doi.org/10.1016/0079-6107(88)90009-0.

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16

Baum, Victor c., and Glenn T. Wetzel. "Sodium-Calcium Exchange in Neonatal Myocardium." Anesthesia & Analgesia 78, no. 6 (June 1994): 1105???1109. http://dx.doi.org/10.1213/00000539-199406000-00012.

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17

Philipson, Kenneth D., and Debora A. Nicoll. "Sodium-Calcium Exchange: A Molecular Perspective." Annual Review of Physiology 62, no. 1 (March 2000): 111–33. http://dx.doi.org/10.1146/annurev.physiol.62.1.111.

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18

De Abajo, F. J., M. A. Serrano-Castro, and P. Sanchez-Garcia. "Sodium-Calcium Exchange and Lithium Action." Journal of Clinical Psychopharmacology 11, no. 4 (August 1991): 279. http://dx.doi.org/10.1097/00004714-199108000-00025.

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19

Eisner, David A., and Karin R. Sipido. "Sodium Calcium Exchange in the Heart." Circulation Research 95, no. 6 (September 17, 2004): 549–51. http://dx.doi.org/10.1161/01.res.0000143419.87518.9e.

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20

O'DAY, PETER A. "Sodium-Calcium Exchange in Invertebrate Photoreceptors." Annals of the New York Academy of Sciences 639, no. 1 Sodium-Calciu (December 1991): 285–99. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17317.x.

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21

CARVALHO, A. P., C. BANDEIRA-DUARTE, I. L. FERREIRA, O. P. COUTINHO, and C. M. CARVALHO. "Sodium-Calcium Exchange in Nerve Terminals." Annals of the New York Academy of Sciences 639, no. 1 Sodium-Calciu (December 1991): 300–311. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17318.x.

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22

CONDRESCU, MADALINA, KWABENA OPUNI, BASIL M. HANTASH, and JOHN P. REEVES. "Cellular Regulation of Sodium-Calcium Exchange." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 214–23. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04744.x.

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23

Reeves, John P. "Molecular aspects of sodium-calcium exchange." Archives of Biochemistry and Biophysics 292, no. 2 (February 1992): 329–34. http://dx.doi.org/10.1016/0003-9861(92)90001-d.

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24

McGuigan, J. A. S., and L. A. Blatter. "Sodium/calcium exchange in ventricular muscle." Experientia 43, no. 11-12 (December 1987): 1140–45. http://dx.doi.org/10.1007/bf01945512.

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25

Pijuan, V., Y. Zhuang, L. Smith, C. Kroupis, M. Condrescu, J. F. Aceto, J. P. Reeves, and J. B. Smith. "Stable expression of the cardiac sodium-calcium exchanger in CHO cells." American Journal of Physiology-Cell Physiology 264, no. 4 (April 1, 1993): C1066—C1074. http://dx.doi.org/10.1152/ajpcell.1993.264.4.c1066.

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A line of Chinese hamster ovary (CHO) cells called CK1.4 was produced by transfection with the gene for the bovine cardiac Na(+)-Ca2+ exchanger. CK1.4 cells stably expressed substantial exchange activity and exchanger protein as shown by immunoprecipitation. Exchange activity was quantified as 45Ca2+ influx that depended on both increasing intracellular Na+ and lowering the concentration of external Na+. Replacing external Na+ with K+ slightly increased 45Ca2+ uptake by CK1.4 cells with basal Na+ and greatly increased 45Ca2+ uptake by Na(+)-loaded cells. Neither exchange activity nor exchanger protein was detected in the nontransfected parental line. By contrast to CK1.4 cells, replacing external Na+ with K+ decreased 45Ca2+ uptake in the nontransfected cells whether or not they were Na+ loaded. Changes in cytosolic free Ca2+ determined with fura-2 were consistent with the 45Ca2+ uptake data. Analysis of poly(A)(+)-RNA by Northern blot confirmed that CK1.4 cells, but not the parental line, expressed the exchangerx. Expression of the exchanger was also observed in aortic myocytes and a renal epithelial cell line (LLC-MK2) but not in other lines of renal epithelial cells (MDCK, LLC-PK1) or human dermal fibroblasts. The cardiac exchanger produced substantial 45Ca2+ efflux from CK1.4 cells in response to hormone-evoked release of stored Ca2+. CK1.4 cells are an attractive model for studies of the regulation of the cardiac exchanger because they stably express sufficient exchanger for biochemical and immunological analysis.

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26

McCarron, John G., John V. Walsh, and Fredric S. Fay. "Sodium/calcium exchange regulates cytoplasmic calcium in smooth muscle." Pflügers Archiv 426, no. 3-4 (February 1994): 199–205. http://dx.doi.org/10.1007/bf00374772.

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27

Palty, Raz, Ehud Ohana, Michal Hershfinkel, Micha Volokita, Vered Elgazar, Ofer Beharier, William F. Silverman, Miriam Argaman, and Israel Sekler. "Lithium-Calcium Exchange Is Mediated by a Distinct Potassium-independent Sodium-Calcium Exchanger." Journal of Biological Chemistry 279, no. 24 (April 1, 2004): 25234–40. http://dx.doi.org/10.1074/jbc.m401229200.

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28

Chernysh, Olga, Madalina Condrescu, and John P. Reeves. "Calcium-dependent regulation of calcium efflux by the cardiac sodium/calcium exchanger." American Journal of Physiology-Cell Physiology 287, no. 3 (September 2004): C797—C806. http://dx.doi.org/10.1152/ajpcell.00176.2004.

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Allosteric regulation by cytosolic Ca2+ of Na+/Ca2+ exchange activity in the Ca2+ efflux mode has received little attention because it has been technically difficult to distinguish between the roles of Ca2+ as allosteric activator and transport substrate. In this study, we used transfected Chinese hamster ovary cells to compare the Ca2+ efflux activities in nontransfected cells and in cells expressing either the wild-type exchanger or a mutant, Δ(241–680), that operates constitutively; i.e., its activity does not require allosteric Ca2+ activation. Expression of the wild-type exchanger did not significantly lower the cytosolic Ca2+ concentration ([Ca2+]i) compared with nontransfected cells. During Ca2+ entry through store-operated Ca2+ channels, Ca2+ efflux by the wild-type exchanger became evident only after [Ca2+]i approached 100–200 nM. A subsequent decline in [Ca2+]i was observed, suggesting that the activation process was time dependent. In contrast, Ca2+ efflux activity was evident under all experimental conditions in cells expressing the constitutive exchanger mutant. After transient exposure to elevated [Ca2+]i, the wild-type exchanger behaved similarly to the constitutive mutant for tens of seconds after [Ca2+]i had returned to resting levels. We conclude that Ca2+ efflux activity by the wild-type exchanger is allosterically activated by Ca2+, perhaps in a time-dependent manner, and that the activated state is briefly retained after the return of [Ca2+]i to resting levels.

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29

Wada, Shin-Ichiro, and Janaki Deepa Weerasooriya. "Sodium-calcium, calcium-potassium, and potassium-sodium exchange equilibria on a montmorillonitic soil." Soil Science and Plant Nutrition 36, no. 3 (July 1990): 451–59. http://dx.doi.org/10.1080/00380768.1990.10416913.

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30

Kline, R. P., L. Zablow, and I. S. Cohen. "Interaction of intracellular ion buffering with transmembrane-coupled ion transport." Journal of General Physiology 95, no. 3 (March 1, 1990): 499–522. http://dx.doi.org/10.1085/jgp.95.3.499.

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The role of the Na/Ca exchanger in the control of cellular excitability and tension development is a subject of current interest in cardiac physiology. It has been suggested that this coupled transporter is responsible for rapid changes in intracellular calcium activity during single beats, generation of plateau currents, which control action potential duration, and control of intracellular sodium during Na/K pump suppression, which may occur during terminal states of ischemia. The actual behavior of this exchanger is likely to be complex for several reasons. First, the exchanger transports two ionic species and thus its instantaneous flux rate depends on both intracellular sodium and calcium activity. Secondly, the alteration in intracellular calcium activity, which is caused by a given transmembrane calcium flux, and which controls the subsequent exchanger rate, is a complex function of available intracellular calcium buffering. The buffers convert the ongoing transmembrane calcium fluxes into changes in activity that are a small and variable fraction of the change in total calcium concentration. Using a number of simple assumptions, we model changes in intracellular calcium and sodium concentration under the influence of Na/Ca exchange, Na/K ATPase and Ca-ATPase pumps, and passive sodium and calcium currents during periods of suppression and reactivation of the Na/K ATPase pump. The goal is to see whether and to what extent general notions of the role of the Na/Ca exchanger used in planning and interpreting experimental studies are consistent with its function as derived from current mechanistic assumptions about the exchanger. We find, for example, that based on even very high estimates of intracellular calcium buffering, it is unlikely that Na/Ca exchange alone can control intracellular sodium during prolonged Na/K pump blockade. It is also shown that Na/Ca exchange can contaminate measurements of Na/K pump currents under a variety of experimental conditions. The way in which these and other functions are affected by the dissociation constants and total capacity of the intracellular calcium buffers are also explored in detail.

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31

Hanson, G. L., W. P. Schilling, and L. H. Michael. "Sodium-potassium pump and sodium-calcium exchange in adult and neonatal canine cardiac sarcolemma." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 2 (February 1, 1993): H320—H326. http://dx.doi.org/10.1152/ajpheart.1993.264.2.h320.

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The purpose of this study was to determine whether the Na(+)-K+ pump and the Na(+)-Ca2+ exchanger, two systems thought to be important in excitation-contraction coupling in the heart, change during postnatal development. In adult and neonatal canine cardiac sarcolemmal preparations, Na(+)-K(+)-adenosine-triphosphatase (ATPase) activity and specific [3H]ouabain binding were found to be higher in the adult compared with the neonate, although Na(+)-K(+)-ATPase turnover numbers were not significantly different. Furthermore, ouabain association and dissociation rate constants, examined under a variety of conditions, were the same for both the neonate and adult preparations. These results suggest that the number of pump units per milligram sarcolemmal protein changes during postnatal development. In contrast, the initial rate of Na(+)-dependent-45Ca2+ influx, an index of Na(+)-Ca2+ exchange activity, was not significantly different in the two age groups. Additionally, the sensitivity of the exchanger to extravesicular Ca2+ and K+ was the same. In summary, during postnatal development sarcolemmal Na(+)-K(+)-ATPase and [3H]ouabain binding increase from neonate to adult, whereas Na(+)-Ca2+ exchange activity remains the same. This may result in a greater importance of Ca2+ flux through the Na(+)-Ca2+ exchange system in the neonate compared with the adult.

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32

Philipson, K. D. "Sodium-Calcium Exchange in Plasma Membrane Vesicles." Annual Review of Physiology 47, no. 1 (October 1985): 561–71. http://dx.doi.org/10.1146/annurev.ph.47.030185.003021.

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33

BLAUSTEIN, MORDECAI P., TERUNAO ASHIDA, WILLIAM F. GOLDMAN, W. WIER, and JOHN M. HAMLYN. "Sodium/Calcium Exchange in Vascular Smooth Muscle:." Annals of the New York Academy of Sciences 488, no. 1 Membrane Path (December 1986): 199–216. http://dx.doi.org/10.1111/j.1749-6632.1986.tb46559.x.

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34

Goldman, WF, PJ Yarowsky, M. Juhaszova, BK Krueger, and MP Blaustein. "Sodium/calcium exchange in rat cortical astrocytes." Journal of Neuroscience 14, no. 10 (October 1, 1994): 5834–43. http://dx.doi.org/10.1523/jneurosci.14-10-05834.1994.

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35

LUCIANI, SISTO, SERGIO BOVA, GABRIELLA CARGNELLI, FEDERICO CUSINATO, and PATRIZIA DEBETTO. "Modulation of Sodium-Calcium Exchange by LipidS." Annals of the New York Academy of Sciences 639, no. 1 Sodium-Calciu (December 1991): 156–65. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17299.x.

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36

WIER, W. GIL. "Sodium-Calcium Exchange in Intact Cardiac Cells." Annals of the New York Academy of Sciences 639, no. 1 Sodium-Calciu (December 1991): 366–74. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17325.x.

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37

MULVANY, M. J., CHRISTIAN AALKJAER, and PETER E. JENSEN. "Sodium-Calcium Exchange in Vascular Smooth Muscle." Annals of the New York Academy of Sciences 639, no. 1 Sodium-Calciu (December 1991): 498–504. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17343.x.

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38

Rybal'chenko, V. K. "Sodium-calcium exchange in small intestinal myocytes." Bulletin of Experimental Biology and Medicine 111, no. 4 (April 1991): 481–84. http://dx.doi.org/10.1007/bf00841480.

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39

Dyer, A., and H. Enamy. "The sodium—calcium exchange in zeolite A." Zeolites 5, no. 2 (March 1985): 66–67. http://dx.doi.org/10.1016/0144-2449(85)90073-9.

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40

Haworth, Robert A., and Atilla B. Goknur. "Inhibition of Sodium/Calcium Exchange and Calcium Channels of Heart Cells by Volatile Anesthetics." Anesthesiology 82, no. 5 (May 1, 1995): 1255–65. http://dx.doi.org/10.1097/00000542-199505000-00021.

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Background Volatile anesthetics exert profound effects on the heart, probably through their effect on Ca2+ movements during the cardiac cycle. Ca2+ movements across the sarcolemma are thought to involve mainly Ca2+ channels and the Na+/Ca2+ exchanger. We have therefore investigated the action of halothane, isoflurane, and enflurane on Na+/Ca2+ exchange and Ca2+ channel activity to assess the contribution of these pathways to the observed effect of the anesthetics on the myocardium. Methods Sarcolemmal ion fluxes were investigated using radioisotope uptake by isolated adult rat heart cells in suspension. Na+/Ca2+ exchange activity was measured from 45Ca2+ uptake by Na(+)-loaded cells. Ca2+ channel activity was measured from verapamil-sensitive trace 54Mn2+ uptake during electric stimulation. Results Halothane, isoflurane, and enflurane inhibited Na+/Ca2+ exchange completely, with similar potency when concentrations were expressed in millimolar units in aqueous medium but not when expressed as minimum alveolar concentration (MAC). The inhibition by enflurane was particularly strong, > 50%, at 2 MAC. In contrast, the three anesthetics inhibited Ca2+ channels with similar potency when concentrations were expressed as MAC but not when expressed in millimolar units in aqueous medium. Hill plots of pooled data with all three anesthetics showed a slope of -3.87 +/- 0.50 for inhibition of Na+/Ca2+ exchange and -1.73 +/- 0.19 for inhibition of Ca2+ channels. Conclusions Halothane, isoflurane, and enflurane inhibit both Na+/Ca2+ exchange and Ca2+ channels at concentrations relevant to anesthesia, although they exhibit differences in potency and number of sites of action. At 1.5 MAC, halothane inhibits Ca2+ channels more than Na+/Ca2+ exchange, whereas enflurane inhibits Na+/Ca2+ exchange more than Ca2+ channels. Isoflurane inhibited both systems equally. The inhibition of Ca2+ influx by these agents is likely to contribute to their negative inotropic effect in the heart. The inhibition of Na+/Ca2+ exchange by enflurane may account for its observed action of delaying relaxation in species lacking sarcoplasmic reticulum.

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41

Opuni, Kwabena, and John P. Reeves. "Feedback Inhibition of Sodium/Calcium Exchange by Mitochondrial Calcium Accumulation." Journal of Biological Chemistry 275, no. 28 (May 2, 2000): 21549–54. http://dx.doi.org/10.1074/jbc.m003158200.

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42

Powis, D. A., K. J. O'Brien, and H. R. K. Von Grafenstein. "Calcium export by sodium-calcium exchange in bovine chromaffin cells." Cell Calcium 12, no. 7 (July 1991): 493–504. http://dx.doi.org/10.1016/0143-4160(91)90031-9.

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43

Smith, J. B., and L. Smith. "Energy dependence of sodium-calcium exchange in vascular smooth muscle cells." American Journal of Physiology-Cell Physiology 259, no. 2 (August 1, 1990): C302—C309. http://dx.doi.org/10.1152/ajpcell.1990.259.2.c302.

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Three different types of mitochondrial poisons (oligomycin, antimycin A, and dinitrophenol) strongly inhibited Na(+)-Ca2+ exchange in aortic myocytes. Exchange activity was assayed as 45Ca2+ uptake that depended on inverting the Na+ gradient and was inhibited by 25 microM dimethylbenzamil. Glucose markedly decreased the inhibition of exchange activity by these three poisons. Glucose also prevented rotenone from inhibiting exchange and depleting cellular ATP. In the absence of glucose, rotenone decreased ATP and exchange activity with half-times of 0.8 and 0.9 min, respectively. Almost eliminating cellular ATP with rotenone maximally inhibited exchange by 80%. Repletion of ATP with glucose substantially restored Na(+)-Ca2+ exchange activity. Ca2+ uptake by organelles, subsequent to entry via exchange for Na+, does not appear to contribute significantly to exchange activity as assayed in intact myocytes. The specific activity of Na(+)-Ca2+ exchange was approximately 30 nmol.min-1.mg protein-1. These findings suggest that ATP modulates exchange activity and that there are approximately 150,000 Na(+)-Ca2+ exchangers per cell, assuming that the turnover number is 1,000 s-1.

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44

Chernysh, Olga, Madalina Condrescu, and John P. Reeves. "Sodium-dependent inactivation of sodium/calcium exchange in transfected Chinese hamster ovary cells." American Journal of Physiology-Cell Physiology 295, no. 4 (October 2008): C872—C882. http://dx.doi.org/10.1152/ajpcell.00221.2008.

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High concentrations of cytosolic Na+ ions induce the time-dependent formation of an inactive state of the Na+/Ca2+ exchanger (NCX), a process known as Na+-dependent inactivation. NCX activity was measured as Ca2+ uptake in fura 2-loaded Chinese hamster ovary (CHO) cells expressing the wild-type (WT) NCX or mutants that are hypersensitive (F223E) or resistant (K229Q) to Na+-dependent inactivation. As expected, 1) Na+-dependent inactivation was promoted by high cytosolic Na+ concentration, 2) the F223E mutant was more susceptible than the WT exchanger to inactivation, whereas the K229Q mutant was resistant, and 3) inactivation was enhanced by cytosolic acidification. However, in contrast to expectations from excised patch studies, 1) the WT exchanger was resistant to Na+-dependent inactivation unless cytosolic pH was reduced, 2) reducing cellular phosphatidylinositol-4,5-bisphosphate levels did not induce Na+-dependent inactivation in the WT exchanger, 3) Na+-dependent inactivation did not increase the half-maximal cytosolic Ca2+ concentration for allosteric Ca2+ activation, 4) Na+-dependent inactivation was not reversed by high cytosolic Ca2+ concentrations, and 5) Na+-dependent inactivation was partially, but transiently, reversed by an increase in extracellular Ca2+ concentration. Thus Na+-dependent inactivation of NCX expressed in CHO cells differs in several respects from the inactivation process measured in excised patches. The refractoriness of the WT exchanger to Na+-dependent inactivation suggests that this type of inactivation is unlikely to be a strong regulator of exchange activity under physiological conditions but would probably act to inhibit NCX-mediated Ca2+ influx during ischemia.

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45

Schoenmakers, T. J. M., P. M. Verbost, G. Flik, and S. E. Wendelaar Bonga. "TRANSCELLULAR INTESTINAL CALCIUM TRANSPORT IN FRESHWATER AND SEAWATER FISH AND ITS DEPENDENCE ON SODIUM/CALCIUM EXCHANGE." Journal of Experimental Biology 176, no. 1 (March 1, 1993): 195–206. http://dx.doi.org/10.1242/jeb.176.1.195.

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Transepithelial calcium uptake and transcellular calcium uptake mechanisms were compared in the proximal intestine of freshwater- and seawater-adapted tilapia, Oreochromis mossambicus. Stripped intestinal epithelium of seawater fish showed a higher paracellular permeability to calcium in vitro. Net transepithelial calcium uptake was 71 % lower, reflecting a physiological response to the increased inward calcium gradient. Na+/K+-ATPase activity was significantly enhanced in enterocytes of seawater-adapted fish, in line with the water transport function of the intestine in seawater fish. The Vmax and the Km values for Ca2+ of the ATP-dependent Ca2+ pump in seawater fish enterocytes were 28 % and 27 %, respectively, lower than in freshwater fish. The Km for Ca2+ of the Na+/Ca2+ exchanger was 22 % lower, and a 57 % decrease in the Vmax for Ca2+ of the exchanger was observed. Apparently, the density of exchanger molecules in the basolateral plasma membrane is reduced in seawater fish. From the correlation between the differences in net intestinal calcium uptake and Na+/Ca2+ exchange activity we conclude that Na+/Ca2+ exchange is the main basolateral effector of transcellular calcium uptake.

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46

Chernaya, Galina, Melissa Vázquez, and John P. Reeves. "Sodium-Calcium Exchange and Store-dependent Calcium Influx in Transfected Chinese Hamster Ovary Cells Expressing the Bovine Cardiac Sodium-Calcium Exchanger." Journal of Biological Chemistry 271, no. 10 (March 8, 1996): 5378–85. http://dx.doi.org/10.1074/jbc.271.10.5378.

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47

Plasman, P. O., P. Lebrun, and A. Herchuelz. "Characterization of the process of sodium-calcium exchange in pancreatic islet cells." American Journal of Physiology-Endocrinology and Metabolism 259, no. 6 (December 1, 1990): E844—E850. http://dx.doi.org/10.1152/ajpendo.1990.259.6.e844.

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Na(+)-Ca2+ exchange may play a role in Ca2+ extrusion from the pancreatic B-cell. The characteristics of the process working in its reverse mode were examined in normal rat pancreatic islet cells. Isosmotical replacement of extracellular Na+ by sucrose induced a concentration-dependent increase in 45Ca uptake, displaying a pharmacological sensitivity compatible with an uptake mediated by Na(+)-Ca2+ exchange. Glucose, up to 2.8 mM, stimulated reverse Na(+)-Ca2+ exchange. Likewise, membrane depolarization activated the process but only under raised intracellular Na+ activity. In conclusion, the B-cell Na(+)-Ca2+ exchange displays properties similar to those observed in other cells: reversibility and sensitivity to membrane potential. When working in its reverse mode the exchanger displays a quite large capacity. The role played by the exchanger in the process of insulin release warrants further investigation.

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48

Hilgemann, D. W., A. Collins, and S. Matsuoka. "Steady-state and dynamic properties of cardiac sodium-calcium exchange. Secondary modulation by cytoplasmic calcium and ATP." Journal of General Physiology 100, no. 6 (December 1, 1992): 933–61. http://dx.doi.org/10.1085/jgp.100.6.933.

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Dynamic responses of cardiac sodium-calcium exchange current to changes of cytoplasmic calcium and MgATP were monitored and analyzed in giant membrane patches excised from guinea pig myocytes. Secondary dependencies of exchange current on cytoplasmic calcium are accounted for in terms of two mechanisms: (a) The sodium-dependent inactivation process, termed I1 modulation, is itself strongly modulated by cytoplasmic calcium. Recovery from the I1 inactivated state is accelerated by increasing cytoplasmic calcium, and the calculated rate of entrance into I1 inactivation is slowed. (b) A second modulation process, termed I2 modulation, is not sodium dependent. As with I1 modulation, the entrance into I2 inactivation takes place over seconds in the absence of cytoplasmic calcium. The recovery from I2 inactivation is a calcium-dependent transition and is rapid (< 200 ms) in the presence of micromolar free calcium. I1 and I2 modulation can be treated as linear, independent processes to account for most exchange modulation patterns observed: (a) When cytoplasmic calcium is increased or decreased in the presence of high cytoplasmic sodium, outward exchange current turns on or off, respectively, on a time scale of multiple seconds. (b) When sodium is applied in the absence of cytoplasmic calcium, no outward current is activated. However, the full outward current is activated within solution switch time when cytoplasmic calcium is applied together with sodium. (c) The calcium dependence of peak outward current attained upon application of cytoplasmic sodium is shifted by approximately 1 log unit to lower concentrations from the calcium dependence of steady-state exchange current. (d) The time course of outward current decay upon decreasing cytoplasmic calcium becomes more rapid as calcium is reduced into the submicromolar range. (e) Under nearly all conditions, the time courses of current decay during application of cytoplasmic sodium and/or removal of cytoplasmic calcium are well fit by single exponentials. Both of the modulation processes are evidently affected by MgATP. Similar to the effects of cytoplasmic calcium, MgATP slows the entrance into I1 inactivation and accelerates the recovery from inactivation. MgATP additionally slows the decay of outward exchange current upon removal of cytoplasmic calcium by 2-10-fold, indicative of an effect on I2 inactivation. Finally, the effects of cytoplasmic calcium on sodium-calcium exchange current are reconstructed in simulations of the I1 and I2 modulation processes as independent reactions.

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Urbanczyk, Jason, Olga Chernysh, Madalina Condrescu, and John P. Reeves. "Sodium-calcium exchange does not require allosteric calcium activation at high cytosolic sodium concentrations." Journal of Physiology 575, no. 3 (September 6, 2006): 693–705. http://dx.doi.org/10.1113/jphysiol.2006.113910.

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50

Sposito, Garrison, and Philip Fletcher. "Sodium-Calcium-Magnesium Exchange Reactions on a Montmorillonitic Soil: III. Calcium-Magnesium Exchange Selectivity." Soil Science Society of America Journal 49, no. 5 (September 1985): 1160–63. http://dx.doi.org/10.2136/sssaj1985.03615995004900050017x.

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