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Journal articles on the topic 'Sarcolemmal Calcium ATPase pump'

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Published: 3 June 2025

Last updated: 31 July 2025

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1

Chen, L. D., P. Kumar, R. J. Reiter, et al. "Melatonin prevents the suppression of cardiac Ca(2+)-stimulated ATPase activity induced by alloxan." American Journal of Physiology-Endocrinology and Metabolism 267, no. 1 (1994): E57—E62. http://dx.doi.org/10.1152/ajpendo.1994.267.1.e57.

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The effects of melatonin treatment on cardiac sarcolemmal membrane function were investigated in alloxan-injected rats. Ca(2+)-stimulated adenosine-triphosphatase (ATPase, Ca2+ pump) and Mg(2+)-ATPase activities were depressed significantly in sarcolemmal preparations from alloxan-injected rats compared with levels in control rats. These deficits were observed 2 days after alloxan injection, and they were accompanied by an increase in the density of voltage-sensitive calcium channels, as measured by the [3H]nitrendipine-binding assay. In a dose-dependent manner, treatment of rats with melatoni

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2

Qu, Yi, Joseph Torchia, and Amar Kumar Sen. "Protein kinase C mediated activation and phosphorylation of Ca2+ pump in cardiac sarcolemma." Canadian Journal of Physiology and Pharmacology 70, no. 9 (1992): 1230–35. http://dx.doi.org/10.1139/y92-171.

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The effects of purified protein kinase C (PKC) on the Ca2+-pumping ATPase of cardiac sarcolemma were investigated. The addition of PKC to sarcolemmal vesicles resulted in a significant increase in ATP-dependent Ca2+ uptake, by increasing the calcium affinity by 2.8-fold (Km 0.14 vs. 0.4 μM for control) and by increasing Vmax from 5 to 6.8 nmol∙mg protein−1∙min−1. The addition of PKC also stimulated Ca2+ ATPase activity in sarcolemmal preparations. This activity was increased further upon the addition of calmodulin. These results suggest that PKC stimulates Ca2+ ATPase through a kinase-directed

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3

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 (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 vari

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4

Saini, Harjot K., and Naranjan S. Dhalla. "Modification of intracellular calcium concentration in cardiomyocytes by inhibition of sarcolemmal Na+/H+ exchanger." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (2006): H2790—H2800. http://dx.doi.org/10.1152/ajpheart.00535.2006.

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Although the Na+/H+ exchanger (NHE) is considered to be involved in regulation of intracellular Ca2+ concentration ([Ca2+]i) through the Na+/Ca2+ exchanger, the exact mechanisms of its participation in Ca2+ handling by cardiomyocytes are not fully understood. Isolated rat cardiomyocytes were treated with or without agents that are known to modify Ca2+ movements in cardiomyocytes and exposed to an NHE inhibitor, 5-( N-methyl- N-isobutyl)amiloride (MIA). [Ca2+]i in cardiomyocytes was measured spectrofluorometrically with fura 2-AM in the absence or presence of KCl, a depolarizing agent. MIA incr

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5

Colston, J. T., P. Kumar, J. P. Chambers, and G. L. Freeman. "Altered sarcolemmal calcium channel density and Ca2+-pump ATPase activity in tachycardia heart failure." Cell Calcium 16, no. 5 (1994): 349–56. http://dx.doi.org/10.1016/0143-4160(94)90028-0.

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6

Piuhola, Jarkko, Annette Hammes, Kai Schuh, Ludwig Neyses, Olli Vuolteenaho, and Heikki Ruskoaho. "Overexpression of sarcolemmal calcium pump attenuates induction of cardiac gene expression in response to ET-1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 3 (2001): R699—R705. http://dx.doi.org/10.1152/ajpregu.2001.281.3.r699.

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The function of the plasma membrane calmodulin-dependent calcium ATPase (PMCA) in myocardium is unknown. PMCA is localized in caveolae, 50- to 100-nm membrane invaginations, which also contain receptors for endothelin-1 (ET-1) and various other ligands. PMCA has been suggested to play a role in regulation of caveolar signal transduction. We studied the effects of the hypertrophic agonist ET-1 and increased coronary perfusion pressure on cardiac synthesis of B-type natriuretic peptide (BNP) in transgenic rats overexpressing the human PMCA 4CI in isolated perfused heart preparation. ET-1 infusio

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7

Kaminishi, T., T. Matsuoka, T. Yanagishita, and K. J. Kako. "Increase vs. decrease of calcium uptake by isolated heart cells induced by H2O2 vs. HOCl." American Journal of Physiology-Cell Physiology 256, no. 3 (1989): C598—C607. http://dx.doi.org/10.1152/ajpcell.1989.256.3.c598.

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Adult rat heart myocytes were labeled rapidly with exogenous [45Ca2+]. Addition of 2.5 mM H2O2 to the heart cell suspension raised the content of rapidly exchangeable intracellular Ca2+ twofold, whereas addition of 1-30 mM HOCl decreased the Ca2+ content. The H2O2-induced increase in Ca2+ content was dependent on the medium Na+, pH, and temperature but was not significantly affected by addition of verapamil, diltiazem, amiloride, or 3-aminobenzamide. The [3H]ouabain binding to myocytes was suppressed by H2O2, whereas the Ca2+ efflux from myocytes was not influenced. An uncoupler, carbonyl cyan

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8

DOWLING, Paul, Philip DORAN, and Kay OHLENDIECK. "Drastic reduction of sarcalumenin in Dp427 (dystrophin of 427 kDa)-deficient fibres indicates that abnormal calcium handling plays a key role in muscular dystrophy." Biochemical Journal 379, no. 2 (2004): 479–88. http://dx.doi.org/10.1042/bj20031311.

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Although the primary abnormality in dystrophin is the underlying cause for mdx (X-chromosome-linked muscular dystrophy), abnormal Ca2+ handling after sarcolemmal microrupturing appears to be the pathophysiological mechanism leading to muscle weakness. To develop novel pharmacological strategies for eliminating Ca2+-dependent proteolysis, it is crucial to determine the fate of Ca2+-handling proteins in dystrophin-deficient fibres. In the present study, we show that a key luminal Ca2+-binding protein SAR (sarcalumenin) is affected in mdx skeletal-muscle fibres. One- and two-dimensional immunoblo

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9

Li, Li, Guoxiang Chu, Evangelia G. Kranias, and Donald M. Bers. "Cardiac myocyte calcium transport in phospholamban knockout mouse: relaxation and endogenous CaMKII effects." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (1998): H1335—H1347. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1335.

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Increases in heart rate are accompanied by acceleration of relaxation. This effect is apparent at the single myocyte level and depends on sarcoplasmic reticulum (SR) Ca transport and Ca/calmodulin dependent protein kinase [CaMKII; see R. A. Bassani, A. Mattiazzi, and D. M. Bers. Am. J. Physiol. 268 ( Heart Circ. Physiol. 37): H703–H712, 1995]. Because phosphorylation of phospholamban (PLB) by CaMKII can stimulate SR Ca transport, it is a plausible candidate mechanism. We examined this issue using ventricular myocytes isolated from wild-type (WT) mice and those in which the PLB gene was ablated

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10

Liu, Jie, Syevda Sirenko, Magdalena Juhaszova, et al. "Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca2+signaling." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 10 (2014): H1385—H1397. http://dx.doi.org/10.1152/ajpheart.00088.2014.

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A reduced sinoatrial node (SAN) functional reserve underlies the age-associated decline in heart rate acceleration in response to stress. SAN cell function involves an oscillatory coupled-clock system: the sarcoplasmic reticulum (SR), a Ca2+clock, and the electrogenic-sarcolemmal membrane clock. Ca2+-activated-calmodulin-adenylyl cyclase/CaMKII-cAMP/PKA-Ca2+signaling regulated by phosphodiesterase activity drives SAN cells automaticity. SR-generated local calcium releases (LCRs) activate Na+/Ca2+exchanger in the membrane clock, which initiates the action potential (AP). We hypothesize that SAN

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11

Kaneko, M., V. Elimban, and N. S. Dhalla. "Mechanism for depression of heart sarcolemmal Ca2+ pump by oxygen free radicals." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 3 (1989): H804—H811. http://dx.doi.org/10.1152/ajpheart.1989.257.3.h804.

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To understand the involvement of changes in sulfhydryl groups in causing depression of the sarcolemmal Ca2+-pump activities, this study was undertaken to examine the effects of oxygen free radicals on rat heart sarcolemmal sulfhydryl groups, Ca2+-stimulated adenosinetriphosphatase (ATPase), and ATP-dependent Ca2+ accumulation. In addition, the effects of sulfhydryl reagents such as dithiothreitol, cysteine, and N-ethylmaleimide on Ca2+-pump activities were investigated. The inhibition of sarcolemmal Ca2+-pump activities by O2-. (xanthine + xanthine oxidase) and H2O2 was decreased by the additi

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12

Kaneko, M., R. E. Beamish, and N. S. Dhalla. "Depression of heart sarcolemmal Ca2+-pump activity by oxygen free radicals." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (1989): H368—H374. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h368.

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Although oxygen free radicals have been implicated as mediators of cellular injury in myocardial ischemia-reperfusion, the exact nature of defects produced by these radicals is not clear. Because sarcolemmal Ca2+-pump is involved in the efflux of Ca2+ from the cell, this study was undertaken to examine the effects of oxygen free radicals on sarcolemmal ATP-dependent Ca2+ accumulation and Ca2+-stimulated Mg2+-dependent adenosinetriphosphatase (ATPase) activities as well as lipid peroxidation of membrane phospholipids. Isolated rat heart sarcolemmal membranes were incubated with xanthine + xanth

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13

McDonough, A. A., and C. A. Schmitt. "Isozymes of dog heart Na+-K+-ATPase are immunologically similar to isozymes in brain." American Journal of Physiology-Cell Physiology 253, no. 6 (1987): C862—C865. http://dx.doi.org/10.1152/ajpcell.1987.253.6.c862.

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The sodium pump, Na+-K+-ATPase, possesses two populations of cardiac glycoside-binding sites in cardiac tissue. This has been observed in other tissues such as brain where the two sites have been assigned to isozymes of Na+-K+-ATPase termed alpha and alpha +. In a previous study [Am. J. Physiol. 248 (Cell Physiol. 17): C247-C251, 1985], we were unable to demonstrate the presence of an alpha +-form in guinea pig heart sarcolemmal membranes using antibody probes. In the present study, using similar methodology, we show that dog, but not rat or guinea pig, sarcolemmal membranes contain two immuno

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14

Pierce, G. N., P. S. Sekhon, H. P. Meng, and T. G. Maddaford. "Effects of chronic swimming training on cardiac sarcolemmal function and composition." Journal of Applied Physiology 66, no. 4 (1989): 1715–21. http://dx.doi.org/10.1152/jappl.1989.66.4.1715.

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Cardiac contractile function is dependent on the integrity and function of the sarcolemmal membrane. Swimming exercise training is known to increase cardiac contractile performance. The purpose of the present study was to examine whether a swimming exercise program would alter sarcolemmal enzyme activity, ion flux, and composition in rat hearts. After approximately 11 wk of exercise training, cardiac myosin and actomyosin Ca2+-adenosinetriphosphatase (ATPase) activity was significantly higher in exercised rat hearts than in sedentary control rat hearts. Glycogen content was increased in planta

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15

Kim, M. S., and T. Akera. "O2 free radicals: cause of ischemia-reperfusion injury to cardiac Na+-K+-ATPase." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 2 (1987): H252—H257. http://dx.doi.org/10.1152/ajpheart.1987.252.2.h252.

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The role of O2 free radicals in the reduction of sarcolemmal Na+-K+-ATPase, which occurs during reperfusion of ischemic heart, was examined in isolated guinea pig heart using exogenous scavengers of O2 radicals and an inhibitor of xanthine oxidase. Ischemia and reperfusion reduced Na+-K+-ATPase activity and specific [3H]ouabain binding to the enzyme in ventricular muscle homogenates and also markedly lowered sodium pump activity estimated from ouabain-sensitive 86Rb+ uptake by ventricular muscle slices. These effects of ischemia and reperfusion were prevented to various degrees by O2-radical s

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16

Zi, Min, Sukhpal Prehar, Elizabeth J. Cartwright, Michael Emerson та Ludwig Neyses. "The sarcolemmal calcium pump modulates β-adrenergic hypertrophic signalling". Journal of Molecular and Cellular Cardiology 40, № 6 (2006): 1003–4. http://dx.doi.org/10.1016/j.yjmcc.2006.03.244.

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17

Makino, N., K. S. Dhalla, V. Elimban, and N. S. Dhalla. "Sarcolemmal Ca2+ transport in streptozotocin-induced diabetic cardiomyopathy in rats." American Journal of Physiology-Endocrinology and Metabolism 253, no. 2 (1987): E202—E207. http://dx.doi.org/10.1152/ajpendo.1987.253.2.e202.

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Heart sarcolemmal membranes were isolated by the sucrose density gradient method from rats with chronic diabetes induced by a streptozotocin (65 mg/kg iv) injection. Na+-dependent Ca2+-uptake activities were significantly depressed in diabetic sarcolemmal membranes; such alterations were evident at different incubation times and at different concentrations of Ca2+. Administration of insulin to diabetic rats normalized the Na+-dependent Ca2+-uptake activities. ATP-dependent Ca2+ accumulation and Ca2+-stimulated Mg2+-dependent ATPase, which represents Ca2+-pump mechanisms, were significantly dep

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18

Dixon, I. M., T. Hata, and N. S. Dhalla. "Sarcolemmal Na(+)-K(+)-ATPase activity in congestive heart failure due to myocardial infarction." American Journal of Physiology-Cell Physiology 262, no. 3 (1992): C664—C671. http://dx.doi.org/10.1152/ajpcell.1992.262.3.c664.

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Because the Na+ pump is considered to modulate the contractile force development by the cardiac muscle and depressed cardiac pump function is the hallmark of congestive heart failure, we characterized the sarcolemmal Na(+)-K(+)-ATPase activity in failing rat hearts after myocardial infarction. For this purpose, the left ventricular coronary artery was ligated, and hearts were examined 4, 8, and 16 wk later; sham-operated animals served as controls. Hemodynamic assessment revealed the presence of abnormal cardiac function at 4, 8, and 16 wk. Although accumulation of ascites in the abdominal cav

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19

Dixon, I. M., T. Hata, and N. S. Dhalla. "Sarcolemmal calcium transport in congestive heart failure due to myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 5 (1992): H1387—H1394. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1387.

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Because Na(+)-Ca2+ exchange and Ca2+ pump are thought to play a role in sarcolemmal Ca2+ movements, we examined the Na(+)-dependent Ca(2+)-uptake and ATP-dependent Ca(2+)-uptake activities in failing heart after myocardial infarction in rats. The left coronary artery was ligated, and the viable left ventricle was used 4, 8, and 16 wk later; sham-operated animals served as controls. Increased left ventricular diastolic pressure and decreased positive and negative change in pressure over time were observed in experimental animals at 4, 8, and 16 wk; these changes were associated with accumulatio

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20

Makino, Naoki, Paul Ganguly, Vijayan Elimban, and Naranjan Dhalla. "Sarcolemmal Alterations in Unloaded Rat Heart after Heterotopic Transplantation." International Journal of Angiology 27, no. 04 (2018): 196–201. http://dx.doi.org/10.1055/s-0038-1673646.

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AbstractFollowing heterotopic transplantation, the rat heart undergoes atrophy and exhibits delayed cardiac relaxation without any changes in contraction and systolic Ca2+ transients. Furthermore, the sarcoplasmic reticular Ca2+ uptake and release activities were reduced and Ca2+ influx through L-type Ca2+ channels was increased in the atrophied heart. Since Ca2+ movements at sarcolemma are intimately involved in the regulation of intracellular Ca2+ concentration, the present study was undertaken to test if sarcolemma plays any role to maintain cardiac function in the atrophied heart.The chara

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21

Nakanishi, H., N. Makino, T. Hata, H. Matsui, K. Yano, and T. Yanaga. "Sarcolemmal Ca2+ transport activities in cardiac hypertrophy caused by pressure overload." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 2 (1989): H349—H356. http://dx.doi.org/10.1152/ajpheart.1989.257.2.h349.

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To examine Ca2+ transport activities in sarcolemmal membrane in cardiac hypertrophy caused by pressure overload, rats were subjected to aortic banding for 28 days. Heart-to-body weight ratio was increased by 46% in aortic-banded animals in comparison with the sham-operated rats. Ouabain-sensitive Na+-K+-ATPase activity in sarcolemma (SL) from hypertrophied hearts was not different from that in the control preparation. The initial rate of Na+-dependent Ca2+ uptake in SL vesicles from the hypertrophied hearts was stimulated by 53% compared with the control vesicles. ATP-dependent Ca2+ uptake and

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22

INUI, M. "Characteristics of phospholamban-calcium pump ATPase system." Journal of Molecular and Cellular Cardiology 24 (May 1992): S31. http://dx.doi.org/10.1016/0022-2828(92)90936-t.

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23

Tian, Jiang, and Zi-jian Xie. "The Na-K-ATPase and Calcium-Signaling Microdomains." Physiology 23, no. 4 (2008): 205–11. http://dx.doi.org/10.1152/physiol.00008.2008.

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The Na-K-ATPase is an energy-transducing ion pump that converts the free energy of ATP into transmembrane ion gradients. It also serves as a functional receptor for cardiotonic steroids such as ouabain and digoxin. Binding of ouabain to the Na-K-ATPase can activate calcium signaling in a cell-specific manner. The exquisite calcium modulation via the Na-K-ATPase is achieved by the ability of the pump to integrate signals from numerous protein and non-protein molecules, including ion transporters, channels, protein kinases/phosphatases, as well as cellular Na+. This review focuses on the unique

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24

Zhang, P., C. Toyoshima, K. Yonekura, G. Inesi, M. Green, and D. L. Stokes. "Structure of the Calcium Pump from Sarcoplasmic Reticulum at 8 Å Resolution: Architecture of the Transmembrane Helices and Localization of the Binding Site for Thapsigargin." Microscopy and Microanalysis 4, S2 (1998): 462–63. http://dx.doi.org/10.1017/s1431927600022431.

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The calcium pump (Ca2+-ATPase) from sarcoplasmic reticulum (SR) is a prominent member of the large family of ATP-dependent cation pumps, which include Na+ /K+-ATPase, H+/K+-ATPase from the stomach, H+-ATPase from yeast and Neurospora, and various detoxifying pumps for Cd+, Cu+ and other metals. In muscle, calcium is stored inside the SR and contraction is initiated by regulated release through specific calcium channels; Ca2+ -ATPase is responsible for relaxation by pumping calcium back into the SR lumen. Many techniques (chemical modification, site mutagenesis, reaction kinetics) have been use

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25

Schuh, Kai, Thomas Quaschning, Sebastian Knauer, et al. "Regulation of Vascular Tone in Animals Overexpressing the Sarcolemmal Calcium Pump." Journal of Biological Chemistry 278, no. 42 (2003): 41246–52. http://dx.doi.org/10.1074/jbc.m307606200.

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26

Harada, Hisato, Barry J. Cusack, Richard D. Olson, et al. "Taurine deficiency and doxorubicin: interaction with the cardiac sarcolemmal calcium pump." Biochemical Pharmacology 39, no. 4 (1990): 745–51. http://dx.doi.org/10.1016/0006-2952(90)90154-d.

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27

CARTWRIGHT, E., K. SCHUH, and L. NEYSES. "Calcium transport in cardiovascular health and disease—The sarcolemmal calcium pump enters the stage." Journal of Molecular and Cellular Cardiology 39, no. 3 (2005): 403–6. http://dx.doi.org/10.1016/j.yjmcc.2005.04.007.

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Enyedi, A., J. Minami, A. J. Caride, and J. T. Penniston. "Characteristics of the Ca2+ pump and Ca2+-ATPase in the plasma membrane of rat myometrium." Biochemical Journal 252, no. 1 (1988): 215–20. http://dx.doi.org/10.1042/bj2520215.

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A plasma membrane-enriched fraction from rat myometrium shows ATP-Mg2+-dependent active calcium uptake which is independent of the presence of oxalate and is abolished by the Ca2+ ionophore A23187. Ca2+ loaded into vesicles via the ATP-dependent Ca2+ uptake was released by extravesicular Na+. This showed that the Na+/Ca2+ exchange and the Ca2+ uptake were both occurring in plasma membrane vesicles. In a medium containing KCl, vanadate readily inhibited the Ca2+ uptake (K1/2 5 microM); when sucrose replaced KCl, 400 microM-vanadate was required for half inhibition. Only a slight stimulation of

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29

Wictome, M., I. Henderson, A. G. Lee, and J. M. East. "Mechanism of inhibition of the calcium pump of sarcoplasmic reticulum by thapsigargin." Biochemical Journal 283, no. 2 (1992): 525–29. http://dx.doi.org/10.1042/bj2830525.

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The steady-state ATPase activity of sarcoplasmic-reticulum (Ca(2+)-Mg2+)-ATPase is inhibited by thapsigargin at a molar ratio of 1:1, with a dissociation constant for thapsigargin estimated to be in the sub-nanomolar range. In the presence of thapsigargin, only a single Ca2+ ion binds to the ATPase. Similarly, addition of thapsigargin to the ATPase incubated in the presence of Ca2+ results in the release of one of the two originally bound Ca2+ ions. As monitored by the fluorescence of nitrobenzo-2-oxa-1,3-diazole-labelled ATPase, thapsigargin appears to shift the transition between E1 and E2 c

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Kumar, R., JT Penniston, and JL Borke. "Ca2+-Mg2+-ATPase Calcium Pumps in the Kidney." Physiology 3, no. 5 (1988): 219–22. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.219.

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Epitopes of the calmodulin-sensitive erythrocyte Ca2+-Mg2+-ATPase enzyme were found exclusively in basolateral membranes of distal tubule cells of the human and rat kidney;other kidney segments did not contain this enzyme in detectable amounts. The calmodulin-sensitive Ca2+-Mg2+-ATPase acts as a calcium pump in the red cell and other tissues. Its presence in the kidney distal tubule, a site where hormone-sensitive calcium transport is known to occur, raises the possibility that this enzyme may act as a hormone-regulated pump in this nephron segment.

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Hammes, Annette, Silke Oberdorf-Maass, Tobias Rother, et al. "Overexpression of the Sarcolemmal Calcium Pump in the Myocardium of Transgenic Rats." Circulation Research 83, no. 9 (1998): 877–88. http://dx.doi.org/10.1161/01.res.83.9.877.

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32

Kitay, Alice Miriam, Marie-Therese Schneebacher, Anne Schmitt, et al. "Modulations in extracellular calcium lead to H+-ATPase-dependent acid secretion: a clarification of PPI failure." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 1 (2018): G36—G42. http://dx.doi.org/10.1152/ajpgi.00132.2017.

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The H+,K+-ATPase was identified as the primary proton secretory pathway in the gastric parietal cell and is the pharmacological target of agents suppressing acid secretion. Recently, we identified a second acid secretory protein expressed in the parietal cell, the vacuolar H+-ATPase (V-type ATPase). The aim of the present study was to further characterize H+-ATPase activation by modulations in extracellular calcium via the calcium sensing receptor (CaSR). Isolated gastric glands were loaded with the pH indicator dye BCECF-AM [2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein acetoxymethy

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Burmeister Getz, E. E., and S. L. Lehman. "Calcium removal kinetics of the sarcoplasmic reticulum ATPase in skeletal muscle." American Journal of Physiology-Cell Physiology 272, no. 4 (1997): C1087—C1098. http://dx.doi.org/10.1152/ajpcell.1997.272.4.c1087.

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The models of the sarcoplasmic reticulum (SR) Ca pump used to simulate Ca kinetics in muscle fibers are simple but inconsistent with data on Ca binding or steady-state uptake. We develop a model of the SR pump that is consistent with data on transient and steady-state Ca removal and has rate constants identified under near-physiological conditions. We also develop models of the other main Ca-binding proteins in skeletal muscle: troponin C and parvalbumin. These models are used to simulate Ca transients in cut fibers during and after depolarizing pulses. Simulations using the full SR pump model

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Siegmund, B., Y. V. Ladilov, and H. M. Piper. "Importance of sodium for recovery of calcium control in reoxygenated cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (1994): H506—H513. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h506.

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The role of Na+ in the recovery from severe anoxic Ca2+ overload was investigated in isolated quiescent ventricular cardiomyocytes from adult rat. Changes of cytosolic Ca2+ and Na+ concentrations were followed by the fura 2 and Na(+)-binding benzofuran isophthalate techniques, respectively. When the fura 2 ratio (340/380 nm) reached saturation in anoxic cells, indicating a severe cytosolic Ca2+ overload, the cells were reoxygenated. This caused a rapid initial drop of cytosolic Ca2+ to a lower but still elevated level (phase I), followed by oscillatory Ca2+ transients at this level (phase II)

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Pappas, G. D., and V. Kriho. "Nerve terminal plasma membrane localization of Ca++-Mg++ ATPase." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 772–73. http://dx.doi.org/10.1017/s0424820100128171.

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Depolarization of the frog neuromuscular junction results In an Influx of calcium from the extracellular space. The cell calcium concentration is increased several fold and release of neurotransmitter results. Following depolarization, a necessity exists for an outwardly directed calcium pump to return the intracellular Ca++ concentration to resting levels. A calcium pump such as this has been described In the erthrocyte plasma membrane as well as In synaptosomal plasma membrane from guinea pig, synaptic membrane fractions from rat cerebral cortex and the plasma membrane of mouse neuroblastoma

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Kaila, K., R. D. Vaughan-Jones, and C. Bountra. "Regulation of intracellular pH in sheep cardiac Purkinje fibre: interactions among Na+, H+ and Ca2+." Canadian Journal of Physiology and Pharmacology 65, no. 5 (1987): 963–69. http://dx.doi.org/10.1139/y87-153.

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Experiments were performed on sheep cardiac Purkinje fibres using pH- and sodium-selective microelectrodes, while simultaneously measuring tension, to determine if the fall in intracellular pH (pHi) following a rise in intracellular Na+ activity [Formula: see text] is caused by inhibition or reversal of acid extrusion on Na+–H+ exhange. A rise in [Formula: see text] was induced either by using the cardioactive steroid strophanthidin to inhibit the sarcolemmal Na+–K+ pump or by increasing the frequency of stimulation (0–4 Hz). Both of these manoeuvres led to an increase in [Formula: see text] a

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Helwig, Bryan, Katherine M. Schreurs, Joslyn Hansen, et al. "Training-induced changes in skeletal muscle Na+-K+ pump number and isoform expression in rats with chronic heart failure." Journal of Applied Physiology 94, no. 6 (2003): 2225–36. http://dx.doi.org/10.1152/japplphysiol.00279.2002.

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The mechanisms responsible for the decrements in exercise performance in chronic heart failure (CHF) remain poorly understood, but it has been suggested that sarcolemmal alterations could contribute to the early onset of muscular fatigue. Previously, our laboratory demonstrated that the maximal number of ouabain binding sites (Bmax) is reduced in the skeletal muscle of rats with CHF (Musch TI, Wolfram S, Hageman KS, and Pickar JG. J Appl Physiol 92: 2326–2334, 2002). These reductions may coincide with changes in the Na+-K+-ATPase isoform (α and β) expression. In the present study, we tested th

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Baba, Akiyasu, Tsutomu Yoshikawa, Michikado Iwata, et al. "Antigen-specific effects of autoantibodies against sarcolemmal Na–K-ATPase pump in immunized cardiomyopathic rabbits." International Journal of Cardiology 112, no. 1 (2006): 15–20. http://dx.doi.org/10.1016/j.ijcard.2006.05.026.

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Horisberger, J. D. "Recent Insights into the Structure and Mechanism of the Sodium Pump." Physiology 19, no. 6 (2004): 377–87. http://dx.doi.org/10.1152/physiol.00013.2004.

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The sodium pump (or Na-K-ATPase) is essential to the function of animal cells. Publication of the related calcium pump (SERCA) structure together with several recent results from a variety of approaches allow us to propose a mechanistic model to answer the question: “How does the sodium pump pump?”

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Ray, Tushar. "The gastric H, K-ATPase system also functions as the Na, K-ATPase and Ca-ATPase in altered states." F1000Research 2 (July 31, 2013): 165. http://dx.doi.org/10.12688/f1000research.2-165.v1.

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This article offers an explanation for the apparent lack of Na, K-ATPase activity in parietal cells although ouabain has been known to inhibit gastric acid secretion since 1962. The gastric H, K-ATPase (proton-pump) seems to be acting in altered states, thus behaving like a Na, K-ATPase (Na-pump) and/or Ca-ATPase (Ca-pump) depending on cellular needs. This conclusion is based on the following findings. First, parietal cell fractions do not exhibit Na, K-ATPase activity at pH 7.0 but do at pH 8.5. Second, the apical plasma membrane (APM) fraction exhibits a (Ca or Mg)-ATPase activity with negli

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Ray, Tushar. "The parietal cell gastric H, K-ATPase also functions as the Na, K-ATPase and Ca-ATPase in altered states." F1000Research 2 (September 12, 2013): 165. http://dx.doi.org/10.12688/f1000research.2-165.v2.

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This article offers an explanation for the apparent lack of Na, K-ATPase activity in parietal cells although ouabain has been known to inhibit gastric acid secretion since 1962. The gastric H, K-ATPase (proton-pump) seems to be acting in altered states, thus behaving like a Na, K-ATPase (Na-pump) and/or Ca-ATPase (Ca-pump) depending on cellular needs. This conclusion is based on the following findings. First, parietal cell fractions do not exhibit Na, K-ATPase activity at pH 7.0 but do at pH 8.5. Second, the apical plasma membrane (APM) fraction exhibits a (Ca or Mg)-ATPase activity with negli

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Zylińska, L., and M. Soszyński. "Plasma membrane Ca2+-ATPase in excitable and nonexcitable cells." Acta Biochimica Polonica 47, no. 3 (2000): 529–39. http://dx.doi.org/10.18388/abp.2000_3976.

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There is a significant number of data confirming that the maintenance of calcium homeostasis in a living cell is a complex, multiregulated process. Calcium efflux from excitable cells (i.e., neurons) occurs through two main systems--an electrochemically driven Na+/Ca2+ exchanger with a low Ca2+ affinity (K0.5 = 10-15 microM), and a plasmalemmal, specific Ca2+-ATPase, with a high Ca2+ affinity (K0.5 < 0.5-1 microM), whereas in nonexcitable cells (i.e., erythrocytes) the calcium pump is the sole system responsible for the extrusion of calcium ions. The plasma membrane Ca2+-ATPase (PMCA) is a

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Green, H. J., E. R. Chin, M. Ball-Burnett, and D. Ranney. "Increases in human skeletal muscle Na(+)-K(+)-ATPase concentration with short-term training." American Journal of Physiology-Cell Physiology 264, no. 6 (1993): C1538—C1541. http://dx.doi.org/10.1152/ajpcell.1993.264.6.c1538.

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To investigate the effect of short-term training on Na(+)-K(+)-adenosine triphosphatase (ATPase) concentration in skeletal muscle and on plasma K+ homeostasis during exercise, 9 subjects performed cycle exercise for 2 h per day for 6 consecutive days at 65% of maximal aerobic power (VO2 max). Na(+)-K(+)-ATPase concentration determined from biopsies obtained from the vastus lateralis muscle using the [3H]ouabain-binding technique increased 13.6% (P < 0.05) as a result of the training (339 +/- 16 vs. 385 +/- 19 pmol/g wet wt, means +/- SE). Increases in Na(+)-K(+)-ATPase concentration were ac

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SUJU, Meylin, Marbelly DAVILA, German POLEO, Roberto DOCAMPO, and Gustavo BENAIM. "Phosphatidylethanol stimulates the plasma-membrane calcium pump from human erythrocytes." Biochemical Journal 317, no. 3 (1996): 933–38. http://dx.doi.org/10.1042/bj3170933.

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Phosphatidylethanol is formed by ‘transphosphatidylation’ of phospholipids with ethanol catalysed by phospholipase D and can be accumulated in the plasma membrane of mammalian cells after treatment of animals with ethanol. In the present work we show that phosphatidylalcohols, such as phosphatidylethanol and phosphatidylbutanol, produced a twofold stimulation of the Ca2+-ATPase activity of human erythrocytes. This stimulation occurs with the purified, solubilized enzyme as well as with ghost preparations, where the enzyme is in its natural lipidic environment and is different to that obtained

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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 (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 tw

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Aubier, M., and N. Viires. "Calcium ATPase and respiratory muscle function." European Respiratory Journal 11, no. 3 (1998): 758–66. http://dx.doi.org/10.1183/09031936.98.11030758.

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The sarcoplasmic reticulum (SR) of striated muscle is a highly specialized intracellular membrane system that plays a key role in the contraction-relaxation cycle of muscle. Its primary function is the regulation of cytoplasmic Ca2+ concentration. A key element in this regulation is the Sarco(endo)plasmic reticulum Ca2+-adenosine triphosphatase (SERCA), which by sequestering Ca2+ into the SR, induces and maintains relaxation. It has been extensively studied with respect to structure and mechanism of action, and more recently to gene expression. Three separate genes encode five SERCA isoforms,

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González Flecha, F. L., P. R. Castello, A. J. Caride, J. J. Gagliardino, and J. P. Rossi. "The erythrocyte calcium pump is inhibited by non-enzymic glycation: studies in situ and with the purified enzyme." Biochemical Journal 293, no. 2 (1993): 369–75. http://dx.doi.org/10.1042/bj2930369.

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In a previous paper we demonstrated that incubation of either intact erythrocytes or erythrocytes membranes with glucose decreases the activity of the membrane Ca(2+)-ATPase [González Flecha, Bermúdez, Cédola, Gagliardino and Rossi (1990) Diabetes 39, 707-711]. The aim of the present work was to obtain information about the mechanism of this inhibition. For this purpose, experiments were carried out with purified Ca(2+)-ATPase, inside-out vesicles and membranes from human erythrocytes. Incubation of the purified Ca(2+)-ATPase with glucose led to a decay in the enzyme activity of up to 50% of t

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FRANKLIN, Isobel K., Robert A. WINZ, and Michael J. HUBBARD. "Endoplasmic reticulum Ca2+-ATPase pump is up-regulated in calcium-transporting dental enamel cells: a non-housekeeping role for SERCA2b." Biochemical Journal 358, no. 1 (2001): 217–24. http://dx.doi.org/10.1042/bj3580217.

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Dental enamel-forming cells face a major challenge to avoid the cytotoxic effects of excess calcium. We have characterized sarcoplasmic/endoplasmic reticulum calcium-ATPase pumps (SERCA) in rat enamel cells to address the proposal that non-mitochondrial calcium stores play a dominant role in transcellular calcium transport. A single major isoform, SERCA2b, was detected during the protein-secretory and calcium-transport stages of enamel formation using reverse-transcriptase PCR, cDNA cloning, Northern analysis and immunoblotting. Most importantly, SERCA2b exhibited a specific 3-fold up-regulati

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Borke, J. L., A. Caride, A. K. Verma, J. T. Penniston, and R. Kumar. "Plasma membrane calcium pump and 28-kDa calcium binding protein in cells of rat kidney distal tubules." American Journal of Physiology-Renal Physiology 257, no. 5 (1989): F842—F849. http://dx.doi.org/10.1152/ajprenal.1989.257.5.f842.

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In an effort to extend our studies on Ca2+ pumps to animal models, we developed a new monoclonal antibody (5F10) prepared against the human erythrocyte Ca2+-Mg2+-adenosinetriphosphatase (ATPase) that recognizes a protein of approximately 140 kDa in rat kidney homogenates. Enzyme-linked immunosorbent assays show that monoclonal antibody 5F10 binds purified Ca2+-Mg2+-ATPase and rat kidney membrane extracts in a concentration-dependent manner. In paraffin-embedded tissue sections, antibody 5F10 binds to an epitope in the basolateral membranes of rat kidney distal convoluted tubule principal cells

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Ren, Bin, Qiming Shao, Pallab K. Ganguly, Paramjit S. Tappia, Nobuakira Takeda, and Naranjan S. Dhalla. "Influence of long-term treatment of imidapril on mortality, cardiac function, and gene expression in congestive heart failure due to myocardial infarction." Canadian Journal of Physiology and Pharmacology 82, no. 12 (2004): 1118–27. http://dx.doi.org/10.1139/y04-115.

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Although it is generally accepted that the efficacy of imidapril, an angiotensin-converting enzyme inhibitor, in congestive heart failure (CHF) is due to improvement of hemodynamic parameters, the significance of its effect on gene expression for sarcolemma (SL) and sarcoplasmic reticulum (SR) proteins has not been fully understood. In this study, we examined the effects of long-term treatment of imidapril on mortality, cardiac function, and gene expression for SL Na+/K+ ATPase and Na+–Ca2+ exchanger as well as SR Ca2+ pump ATPase, Ca2+ release channel (ryanodine receptor), phospholamban, and

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