Development of a linear transient model for stimulation of isolated cardiac cells

2000 ◽  
Vol 12 (3) ◽  
pp. 217-222 ◽  
Author(s):  
P. Pham ◽  
G. Cauffet ◽  
A. Bardou ◽  
J. Olivares ◽  
E. Novakov
Keyword(s):  
Cardiac Cells ◽  
Transient Model ◽  
Isolated Cardiac Cells ◽  
Stimulation Of

scholarly journals Potential cytotoxicity of silver nanoparticles: Stimulation of autophagy and mitochondrial dysfunction in cardiac cells

2021 ◽  
Author(s):  
Azmat Ali Khan ◽  
Amer M. Alanazi ◽  
Nawaf Alsaif ◽  
Mohammad Al-anazi ◽  
Ahmed Y.A. Sayed ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Mitochondrial Dysfunction ◽  
Cardiac Cells ◽  
Stimulation Of

Electrophysiology of the Sodium-Potassium-ATPase in Cardiac Cells

2001 ◽  
Vol 81 (4) ◽  
pp. 1791-1826 ◽  
Author(s):  
Helfried Günther Glitsch
Keyword(s):  
Cell Membrane ◽  
Potential Gradient ◽  
Outward Current ◽  
Pump Current ◽  
Cardiac Cells ◽  
Animal Cells ◽  
Excitable Cells ◽  
Extracellular Medium ◽  
Enzymatic Isolation ◽  
Isolated Cardiac Cells

Like several other ion transporters, the Na+-K+ pump of animal cells is electrogenic. The pump generates the pump current I p. Under physiological conditions, I p is an outward current. It can be measured by electrophysiological methods. These methods permit the study of characteristics of the Na+-K+ pump in its physiological environment, i.e., in the cell membrane. The cell membrane, across which a potential gradient exists, separates the cytosol and extracellular medium, which have distinctly different ionic compositions. The introduction of the patch-clamp techniques and the enzymatic isolation of cells have facilitated the investigation of I p in single cardiac myocytes. This review summarizes and discusses the results obtained from I p measurements in isolated cardiac cells. These results offer new exciting insights into the voltage and ionic dependence of the Na+-K+ pump activity, its effect on membrane potential, and its modulation by hormones, transmitters, and drugs. They are fundamental for our current understanding of Na+-K+ pumping in electrically excitable cells.

Modulation of Na + Current Inactivation by Stimulation of Protein Kinase C in Cardiac Cells

1997 ◽  
Vol 81 (3) ◽  
pp. 380-386 ◽  
Author(s):  
Cheryl L. Watson ◽  
Michael R. Gold
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cardiac Cells ◽  
Na Current ◽  
Kinase C ◽  
Stimulation Of

Insulin stimulation of protein synthesis in cultured skeletal and cardiac muscle cells

1982 ◽  
Vol 243 (1) ◽  
pp. C81-C86 ◽  
Author(s):  
J. Airhart ◽  
J. A. Arnold ◽  
W. S. Stirewalt ◽  
R. B. Low
Keyword(s):  
Protein Synthesis ◽  
Specific Activity ◽  
Muscle Cells ◽  
Cell Types ◽  
Cardiac Cells ◽  
Cardiac Muscle Cells ◽  
Significant Stimulation ◽  
Chick Heart ◽  
Embryonic Chick Heart ◽  
Stimulation Of

The effects of acute exposure to insulin on protein synthesis were examined in primary, differentiated cultures of embryonic chick heart and skeletal muscle cells. Synthetic rates were calculated using the specific activity of tRNA-bound leucine as precursor, a specific activity that was significantly less than that of extracellular leucine but greater than that of free, intracellular leucine at 0.2 mM external leucine. Insulin did not alter these relationships. Doses of insulin in the physiological range produced significant stimulation of protein synthesis in both cell types. Maximal responses, involving approximately 30% increases in both absolute and fractional rates, were observed at higher insulin concentrations. Significant stimulation by insulin was seen in cardiac cells after only 1 h of insulin treatment, and the effects of the hormone were observed both in the presence and absence of serum in the culture medium.

Alpha 1-adrenoceptor and purinoceptor agonists modulate Na-H antiport in single cardiac cells

1993 ◽  
Vol 264 (2) ◽  
pp. H310-H319 ◽  
Author(s):  
M. Puceat ◽  
O. Clement-Chomienne ◽  
A. Terzic ◽  
G. Vassort
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cardiac Cells ◽  
Extracellular Medium ◽  
Beta Adrenoceptor ◽  
Kinase C ◽  
Intracellular Ca ◽  
Acid Load ◽  
Ethanesulfonic Acid ◽  
Stimulation Of

We investigated the effects of an alpha 1-adrenoceptor (phenylephrine) and a purinoceptor agonist (ATP), both of which accelerate the phosphoinositide turnover, on the Na-H antiport activity of rat single cardiac cells using the pH-sensitive fluorescent indicator seminaphthorhodafluor-1 (SNARF-1). Both phenylephrine, in the presence of a beta-adrenoceptor blocker, and ATP enhanced the ability of the cell to regulate its intracellular pH (pHi) after an imposed acid load. This effect was observed in HCO3-free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) and prevented by Na-H antiport inhibitors ethylisopropylamiloride (EIPA) or amiloride. Similar results were obtained when cells were bathed in an acidic extracellular medium. Hence, the alpha 1-adrenoceptor and purinoceptor agonists activate the Na-H antiport even when it is partially inhibited by extracellular protons. To further evaluate the effects of the two neurohormones, the rate of proton efflux was estimated as a function of the magnitude of the imposed acid load. The results indicate that the agonist-induced modulation of the Na-H antiport is caused by an acceleration of its exchange activity and by a shift of its dependence on pHi toward more alkaline pH values. The agonist-mediated stimulation of the antiport was also observed in partially depolarized cells and was not dependent on intracellular Ca. Phorbol 12-myristate 13-acetate was not able to reproduce the effects of the agonists on the Na-H antiport. Conversely, the inhibitors of protein kinase C did not prevent the activation of the antiport by the neurohormones. Thus our data suggest that neither a Ca-calmodulin-dependent kinase nor protein kinase C is responsible for the alpha 1-adrenoceptor- and purinoceptor-mediated stimulation of the antiport.

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