scholarly journals The role of stretch, tachycardia and sodium‐calcium exchanger in induction of early cardiac remodelling

2020 ◽  
Vol 24 (15) ◽  
pp. 8732-8743 ◽  
Author(s):  
Natasa Djalinac ◽  
Senka Ljubojevic‐Holzer ◽  
Ingrid Matzer ◽  
Ewald Kolesnik ◽  
Katharina Jandl ◽  
...  
Keyword(s):  
Cardiac Remodelling ◽  
Sodium Calcium Exchanger ◽  
Sodium Calcium

Expression and role of calcium-ATPase pump and sodium-calcium exchanger in differentiated trophoblasts from human term placenta

2003 ◽  
Vol 65 (3) ◽  
pp. 283-288 ◽  
Author(s):  
Robert Moreau ◽  
Georges Daoud ◽  
Andr� Masse ◽  
Lucie Simoneau ◽  
Julie Lafond
Keyword(s):  
Calcium Atpase ◽  
Sodium Calcium Exchanger ◽  
Human Term Placenta ◽  
Term Placenta ◽  
Sodium Calcium

scholarly journals Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

2019 ◽  
Vol 151 (6) ◽  
pp. 786-797 ◽  
Author(s):  
Danna Morales ◽  
Tamara Hermosilla ◽  
Diego Varela
Keyword(s):  
Calcium Current ◽  
Calcium Currents ◽  
Adrenergic Stimulation ◽  
Sodium Calcium Exchanger ◽  
Adrenergic Agonist ◽  
Rat Cardiomyocytes ◽  
Calcium Dependent ◽  
Sodium Calcium ◽  
Dependent Inactivation

The activity of L-type calcium channels is associated with the duration of the plateau phase of the cardiac action potential (AP) and it is controlled by voltage- and calcium-dependent inactivation (VDI and CDI, respectively). During β-adrenergic stimulation, an increase in the L-type current and parallel changes in VDI and CDI are observed during square pulses stimulation; however, how these modifications impact calcium currents during an AP remains controversial. Here, we examined the role of both inactivation processes on the L-type calcium current activity in newborn rat cardiomyocytes in control conditions and after stimulation with the β-adrenergic agonist isoproterenol. Our approach combines a self-AP clamp (sAP-Clamp) with the independent inhibition of VDI or CDI (by overexpressing CaVβ2a or calmodulin mutants, respectively) to directly record the L-type calcium current during the cardiac AP. We find that at room temperature (20–23°C) and in the absence of β-adrenergic stimulation, the L-type current recapitulates the AP kinetics. Furthermore, under our experimental setting, the activity of the sodium–calcium exchanger (NCX) does not affect the shape of the AP. We find that hindering either VDI or CDI prolongs the L-type current and the AP in parallel, suggesting that both inactivation processes modulate the L-type current during the AP. In the presence of isoproterenol, wild-type and VDI-inhibited cardiomyocytes display mismatched L-type calcium current with respect to their AP. In contrast, CDI-impaired cells maintain L-type current with kinetics similar to its AP, demonstrating that calcium-dependent inactivation governs L-type current kinetics during β-adrenergic stimulation.

Role of the Sodium-calcium Exchanger (NCX-1) within Splotch (Sp2h) Myocardial Failure

2007 ◽  
pp. 193-195
Author(s):  
Jian Wang ◽  
Andrew Lindsley ◽  
Tony Creazzo ◽  
Srinagesh V. Koushik ◽  
Simon J. Conway
Keyword(s):  
Sodium Calcium Exchanger ◽  
Myocardial Failure ◽  
Sodium Calcium

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.

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