The role of intracellular sodium ions in the regulation of cardiac contractility

1982 ◽  
Vol 14 (3) ◽  
pp. 189-192 ◽  
Author(s):  
J Daut
Keyword(s):  
Cardiac Contractility ◽  
Intracellular Sodium ◽  
Sodium Ions

The role of sodium ions in the thermoluminescence peaks of laboratory-irradiated natural quartz

2021 ◽  
Vol 141 ◽  
pp. 106539
Author(s):  
Tran Ngoc ◽  
Ho Van Tuyen ◽  
Le Anh Thi ◽  
Le Xuan Hung ◽  
Nguyen Xuan Ca ◽  
...  
Keyword(s):  
Sodium Ions ◽  
Natural Quartz

scholarly journals What Density of Magnetosheath Sodium Ions Can Provide the Observed Decrease in the Magnetic Field of the “Double Magnetopause” during the First MESSENGER Flyby?

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1168
Author(s):  
Elena Belenkaya ◽  
Ivan Pensionerov
Keyword(s):  
Magnetic Field ◽  
Analytical Approach ◽  
Field Structure ◽  
Sodium Ions ◽  
Plasma Parameters ◽  
Calculation Results ◽  
Magnetizing Current ◽  
The Magnetic Field ◽  
Density Excess

On 14 January 2008, the MESSENGER spacecraft, during its first flyby around Mercury, recorded the magnetic field structure, which was later called the “double magnetopause”. The role of sodium ions penetrating into the Hermean magnetosphere from the magnetosheath in generation of this structure has been discussed since then. The violation of the symmetry of the plasma parameters at the magnetopause is the cause of the magnetizing current generation. Here, we consider whether the change in the density of sodium ions on both sides of the Hermean magnetopause could be the cause of a wide diamagnetic current in the magnetosphere at its dawn-side boundary observed during the first MESSENGER flyby. In the present paper, we propose an analytical approach that made it possible to determine the magnetosheath Na+ density excess providing the best agreement between the calculation results and the observed magnetic field in the double magnetopause.

scholarly journals Advances in understanding the role of cardiac glycosides in control of sodium transport in renal tubules

2014 ◽  
Vol 222 (1) ◽  
pp. R11-R24 ◽  
Author(s):  
Syed Jalal Khundmiri
Keyword(s):  
Heart Failure ◽  
Intracellular Signaling ◽  
Cardiac Contractility ◽  
Myocardial Cell ◽  
Renal Tubules ◽  
Intracellular Signaling Pathway ◽  
Body Sodium ◽  
Membrane Bound ◽  
Total Body

Cardiotonic steroids have been used for the past 200 years in the treatment of congestive heart failure. As specific inhibitors of membrane-bound Na+/K+ATPase, they enhance cardiac contractility through increasing myocardial cell calcium concentration in response to the resulting increase in intracellular Na concentration. The half-minimal concentrations of cardiotonic steroids required to inhibit Na+/K+ATPase range from nanomolar to micromolar concentrations. In contrast, the circulating levels of cardiotonic steroids under physiological conditions are in the low picomolar concentration range in healthy subjects, increasing to high picomolar levels under pathophysiological conditions including chronic kidney disease and heart failure. Little is known about the physiological function of low picomolar concentrations of cardiotonic steroids. Recent studies have indicated that physiological concentrations of cardiotonic steroids acutely stimulate the activity of Na+/K+ATPase and activate an intracellular signaling pathway that regulates a variety of intracellular functions including cell growth and hypertrophy. The effects of circulating cardiotonic steroids on renal salt handling and total body sodium homeostasis are unknown. This review will focus on the role of low picomolar concentrations of cardiotonic steroids in renal Na+/K+ATPase activity, cell signaling, and blood pressure regulation.

The Role of Additives in the Electroreduction of Sodium Ions in Chloroaluminate-Based Ionic Liquids

2005 ◽  
Vol 152 (1) ◽  
pp. E9 ◽  
Author(s):  
Ketack Kim ◽  
Christopher Lang ◽  
Paul A. Kohl
Keyword(s):  
Ionic Liquids ◽  
Sodium Ions

Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels

2002 ◽  
Vol 282 (4) ◽  
pp. H1334-H1340 ◽  
Author(s):  
R. R. Lamberts ◽  
M. H. P. van Rijen ◽  
P. Sipkema ◽  
P. Fransen ◽  
S. U. Sys ◽  
...  
Keyword(s):  
Ion Channels ◽  
Perfusion Pressure ◽  
Cardiac Contractility ◽  
No Synthase ◽  
Coronary Perfusion ◽  
Channel Blockade ◽  
No Release ◽  
Sustained Increase ◽  
Stretch Activated Ion Channels

The role of stretch-activated ion channels (SACs) in coronary perfusion-induced increase in cardiac contractility was investigated in isolated isometrically contracting perfused papillary muscles from Wistar rats. A brief increase in perfusion pressure (3–4 s, perfusion pulse, n = 7), 10 repetitive perfusion pulses ( n = 4), or a sustained increase in perfusion pressure (150–200 s, perfusion step, n = 7) increase developed force by 2.7 ± 1.1, 7.7 ± 2.2, and 8.3 ± 2.5 mN/mm2 (means ± SE, P < 0.05), respectively. The increase in developed force after a perfusion pulse is transient, whereas developed force during a perfusion step remains increased by 5.1 ± 2.5 mN/mm2 ( P < 0.05) in the steady state. Inhibition of SACs by addition of gadolinium (10 μmol/l) or streptomycin (40 and 100 μmol/l) blunts the perfusion-induced increase in developed force. Incubation with 100 μmol/l N ω-nitro-l-arginine [nitric oxide (NO) synthase inhibition], 10 μmol/l sodium nitroprusside (NO donation) and 0.1 μmol/l verapamil (L-type Ca2+ channel blockade) are without effect on the perfusion-induced increase of developed force. We conclude that brief, repetitive, or sustained increases in coronary perfusion augment cardiac contractility through activation of stretch-activated ion channels, whereas endothelial NO release and L-type Ca2+channels are not involved.

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