Regulation of calcium transport in cardiac cells

1984 ◽  
Vol 62 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Adil E. Shamoo ◽  
Indu S. Ambudkar
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Transport ◽  
Cardiac Cells ◽  
Transport Systems ◽  
Sodium Calcium Exchanger ◽  
Inotropic Effects ◽  
Cellular Calcium ◽  
Sodium Calcium

Calcium transporting systems and the regulatory events accompanying them are pivotal in the function of the cardiac cell. The concerted involvement of the various membranes achieve cellular calcium homeostasis that can also respond to the physiological exigencies of the cell. Three membrane systems are primarily involved; the sarcolemma, sarcoplasmic reticulum, and the mitochondria. The various Ca2+ transport systems that have been described in these membranes are as follows: the calcium channel, Ca2+-ATPase, Ca2+–Mg2+ ATPase, and sodium–calcium exchanger in the sarcolemma; the Ca2+–Mg2+ ATPase and a possible calcium channel in the sarcoplasmic reticulum; and the sodium–calcium exchanger and electrophoretic calcium uniporter in the mitochondrial inner membrane. These systems mediate calcium fluxes to maintain physiological cytosolic calcium concentrations. β-Adrenergic hormones regulate calcium transport systems in sarcolemma and sarcoplasmic reticulum, while α-adrenergic hormones modulate those in the mitochondria and probably in the sarcolemma. The response to these hormones is initiated at the sarcolemma, which contains the specific receptors. Intracellularly the effects are propagated by secondary messengers, e.g., cAMP, calcium, and lipid changes. Specific proteins are also involved in these events. Phospholamban, a 22 000 dalton protein, is involved in mediating the cAMP-dependent inotropic effects, by activating the Ca2+–Mg2+ ATPase of the sarcoplasmic reticulum. Alterations in any one of the systems involved in the regulation of calcium transport or in the calcium transport systems per se, would then result in drastic alterations in the cellular calcium homeostasis. Such effects could be of significance in cellular dysfunction during cardiac disease.

scholarly journals Role of Sodium/Calcium Exchangers in Tumors

Biomolecules ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1257
Author(s):  
Barbora Chovancova ◽  
Veronika Liskova ◽  
Petr Babula ◽  
Olga Krizanova
Keyword(s):  
Cancer Cells ◽  
Calcium Ions ◽  
Calcium Transport ◽  
Current Knowledge ◽  
Transport Systems ◽  
Sodium Ions ◽  
Sodium Calcium Exchanger ◽  
Reverse Mode ◽  
Sodium Calcium

The sodium/calcium exchanger (NCX) is a unique calcium transport system, generally transporting calcium ions out of the cell in exchange for sodium ions. Nevertheless, under special conditions this transporter can also work in a reverse mode, in which direction of the ion transport is inverted—calcium ions are transported inside the cell and sodium ions are transported out of the cell. To date, three isoforms of the NCX have been identified and characterized in humans. Majority of information about the NCX function comes from isoform 1 (NCX1). Although knowledge about NCX function has evolved rapidly in recent years, little is known about these transport systems in cancer cells. This review aims to summarize current knowledge about NCX functions in individual types of cancer cells.

Negative and Positive Inotropic Effects of Propofol via  L-type Calcium Channels and the Sodium-Calcium Exchanger in Rat Cardiac Trabeculae

2002 ◽  
Vol 97 (5) ◽  
pp. 1146-1155 ◽  
Author(s):  
Wouter de Ruijter ◽  
Ger J. M. Stienen ◽  
Jan van Klarenbosch ◽  
Jacob J. de Lange
Keyword(s):  
Calcium Channel ◽  
Calcium Concentration ◽  
Positive Inotropic Effect ◽  
Calcium Influx ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Sodium Calcium Exchanger ◽  
Inotropic Effects ◽  
Reverse Mode ◽  
Sodium Calcium

Background Conflicting opinions are present in the literature regarding the origin of the negative inotropic effect of propofol on the myocardium. This study aims to resolve these discrepancies by investigating the inotropic effects of propofol the L-type calcium channels and the sodium-calcium exchanger (NCX). Methods The effect of 20 microg/ml propofol on force development was determined in rat cardiac trabeculae at different pacing frequencies and different extracellular calcium concentrations. Postrest potentiation, sodium withdrawal during quiescence, and the NCX inhibitor KB-R7943 were used to study changes in the activity of the reverse mode of the NCX by propofol. Results The effect of propofol on steady state peak force depended on pacing frequency and calcium concentration. A negative inotropic effect was observed at pacing frequencies greater than 0.5 Hz, but a positive inotropic effect was observed at 0.1 Hz and low calcium, which cannot be explained by an effect on the L-type calcium channel. Propofol enhanced postrest potentiation in a calcium-dependent manner. Sodium withdrawal during quiescence and the use of the specific NCX inhibitor KB-R7943 provided evidence for an enhancement of calcium influx by propofol the reverse mode of the NCX. Conclusions The effects of propofol on the myocardium depend on pacing frequency and calcium concentration. The positive inotropic effect of propofol is associated with increased calcium influx the reverse mode of the NCX. The authors conclude that the net inotropic effect of propofol is the result of its counteracting influence on the functioning of the L-type calcium channel and the NCX.

scholarly journals Burn trauma alters calcium transporter protein expression in the heart

2004 ◽  
Vol 97 (4) ◽  
pp. 1470-1476 ◽  
Author(s):  
Cherry Ballard-Croft ◽  
Deborah Carlson ◽  
David L. Maass ◽  
Jureta W. Horton
Keyword(s):  
Calcium Channel ◽  
Ryanodine Receptor ◽  
Burn Injury ◽  
Calcium Handling ◽  
Sodium Calcium Exchanger ◽  
Sodium Potassium ◽  
Burn Trauma ◽  
Sodium Calcium ◽  
Transporter Expression ◽  
Calcium Transporter

We have shown previously that burn trauma produces significant cardiac dysfunction, which is first evident 8 h postburn and is maximal 24 h postburn. Because calcium handling by the cardiomyocyte is essential for cardiac function, one mechanism by which burn injury may cause cardiac abnormalities is via calcium dyshomeostasis. We hypothesized that major burn injury alters cardiomyocyte calcium handling through changes in calcium transporter expression. Sprague-Dawley rats were given either burn injury or no burn injury (controls). Cardiomyocyte intracellular calcium and sodium were quantified at various times postburn by fura 2-AM or sodium-binding benzofuran isophthalate fluorescent indicators, respectively. In addition, hearts freeze-clamped at various times postburn (2, 4, 8, and 24 h) were used for Western blot analysis using antibodies against the sarcoplasmic reticulum calcium-ATPase (SERCA), the L-type calcium-channel, the ryanodine receptor, the sodium/calcium exchanger, or the sodium-potassium-ATPase. Intracellular calcium levels were elevated significantly 8–24 h postburn, and intracellular sodium was increased significantly 4 through 24 h postburn. Expression of SERCA was significantly reduced 1–8 h postburn, whereas L-type calcium-channel expression was diminished 1 and 2 h postburn ( P < 0.05) but returned toward control levels 4 h postburn. Ryanodine receptor protein was significantly reduced at 1 and 2 h postburn, returning to baseline by 4 h postburn. Sodium/calcium exchanger expression was significantly elevated 2 h postburn but was significantly reduced 24 h postburn. An increase in sodium-potassium-ATPase expression occurred 2–24 h postburn. These data confirm that burn trauma alters calcium transporter expression, likely contributing to cardiomyocyte calcium loading and cardiac contractile dysfunction.

scholarly journals Effect of Verapamil, an L-Type Calcium Channel Inhibitor, on Caveolin-3 Expression in Septic Mouse Hearts

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Bruna A. C. Rattis ◽  
Ana C. Freitas ◽  
Jordana F. Oliveira ◽  
João L. A. Calandrini-Lima ◽  
Maria J. Figueiredo ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Myocardial Dysfunction ◽  
Vital Role ◽  
Cardiac Cells ◽  
Structural Protein ◽  
Cardiac Muscle Cells ◽  
Septic Mouse ◽  
Cardiac Lesions

Sepsis-induced myocardial dysfunction considerably increases mortality risk in patients with sepsis. Previous studies from our group have shown that sepsis alters the expression of structural proteins in cardiac cells, resulting in cardiomyocyte degeneration and impaired communication between cardiac cells. Caveolin-3 (CAV3) is a structural protein present in caveolae, located in the membrane of cardiac muscle cells, which regulates physiological processes such as calcium homeostasis. In sepsis, there is a disruption of calcium homeostasis, which increases the concentration of intracellular calcium, which can lead to the activation of potent cellular enzymes/proteases which cause severe cellular injury and death. The purpose of the present study was to test the hypotheses that sepsis induces CAV3 overexpression in the heart, and the regulation of L-type calcium channels directly relates to the regulation of CAV3 expression. Severe sepsis increases the expression of CAV3 in the heart, as immunostaining in our study showed CAV3 presence in the cardiomyocyte membrane and cytoplasm, in comparison with our control groups (without sepsis) that showed CAV3 presence predominantly in the plasma membrane. The administration of verapamil, an L-type calcium channel inhibitor, resulted in a decrease in mortality rates of septic mice. This effect was accompanied by a reduction in the expression of CAV3 and attenuation of cardiac lesions in septic mice treated with verapamil. Our results indicate that CAV3 has a vital role in cardiac dysfunction development in sepsis and that the regulation of L-type calcium channels may be related to its expression.

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