Primary Culture of Human Atrial Myocytes is Associated with the Appearance of Structural and Functional Characteristics of Immature Myocardium

1997 ◽  
Vol 29 (5) ◽  
pp. 1307-1320 ◽  
Author(s):  
Agnès Bénardeau ◽  
Stéphane N. Hatem ◽  
Catherine Rücker-Martin ◽  
Sophie Tessier ◽  
Sylvie Dinanian ◽  
...  
Keyword(s):  
Primary Culture ◽  
Atrial Myocytes ◽  
Functional Characteristics ◽  
Human Atrial Myocytes ◽  
Immature Myocardium

Properties of sodium and potassium currents of cultured adult human atrial myocytes

1996 ◽  
Vol 270 (5) ◽  
pp. H1676-H1686 ◽  
Author(s):  
J. Feng ◽  
G. R. Li ◽  
B. Fermini ◽  
S. Nattel
Keyword(s):  
Primary Culture ◽  
Molecular Mechanisms ◽  
Voltage Dependence ◽  
Phenotypic Expression ◽  
Ionic Currents ◽  
Delayed Rectifier ◽  
Atrial Myocytes ◽  
Qualitative Properties ◽  
Human Atrial Myocytes ◽  
Electrophysiological Properties

Cultured cell systems are valuable for the study of regulation of phenotypic expression, but little is known about the electrophysiological properties of human cardiac tissues in culture. The present studies were designed to determine the feasibility of maintaining human atrial myocytes in primary culture and to assess changes in Na+ (INa) and K+ (Ito, transient outward, and Ikur, ultra-rapid delayed rectifier) currents. Within 24 h of culture, cells assumed an avoid shape, which they maintained for up to 7 days. The voltage dependence, kinetics, and density of INa were unchanged in culture. The activation properties of Ito (kinetics and voltage dependence) were not altered, but Ito density (current normalized to cell capacitance) was reduced and inactivation properties were altered (negative shift in voltage dependence and slowed kinetics) in cultured compared with fresh cells. The absolute current amplitude, kinetics, voltage dependence, and 4-aminopyridine sensitivity of IKur were unchanged, but current density was increased. All changes in ionic currents occurred within 24 h of culture and remained stable for the next 4 days. We conclude that human atrial myocytes can be maintained in primary culture, that the qualitative properties of INa, Ito, and IKur remain constant but that some quantitative changes occur, and that cultured human atrial myocytes may be valuable for studies of the molecular mechanisms and regulation of cardiac channel function in humans.

scholarly journals Sarcoplasmic reticulum and L-type Ca2+channel activity regulate the beat-to-beat stability of calcium handling in human atrial myocytes

2011 ◽  
Vol 589 (13) ◽  
pp. 3247-3262 ◽  
Author(s):  
Anna Llach ◽  
Cristina E. Molina ◽  
Jacqueline Fernandes ◽  
Josep Padró ◽  
Juan Cinca ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Handling ◽  
Channel Activity ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes

P2863Regional specific remodeling of cGMP pathway in human atrial fibrillation

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N I Bork ◽  
N G Pavlidou ◽  
B Reiter ◽  
H Reichenspurner ◽  
T Christ ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Sinus Rhythm ◽  
Ryanodine Receptors ◽  
Membrane Receptors ◽  
Mrna Levels ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Cgmp Pathway ◽  
The Right

Abstract Background Atrial fibrillation (AF) is accompanied by a profound remodeling of membrane receptors and alterations in cyclic nucleotides-dependent regulation of Ca2+-handling. Thus, while basal ryanodine receptors activity is upregulated, L-type calcium current (ICa,L) density is diminish in AF, due to local microdomain-specific cAMP dynamics. The same seems true for cGMP regulation in AF. In AF cGMP-mediated increase in ICa,L is blunted but NO-mediated attenuation of β-adrenoceptors stimulation-mediated increase is preserved. However, although the role of cGMP in controling atrial function and pathophysiology is controversial, no study has been ever performed in human myocytes to measure cGMP directly. Methods We isolated myocytes from the right and/or left atrium of 27 patients in sinus rhythm (SR), and with AF. Cells were then transfected with adenovirus to express the cytosolic FRET-based cGMP sensor red-cGES-DE5 and cultured for 48 hours. Förster resonance energy transfer (FRET) was used to measure cGMP in 61 living human atrial myocytes. We stimulated cells with the C-type natriuretic peptide CNP (100 nM and 1 μM), and the non-selective phosphodiesterases (PDEs) inhibitor IBMX (100 μM). Additionally, PDE specific inhibitors for PDE2 (Bay 60–7550, 100 nM) and PDE3 (Cilostamide, 10 μM) as well as inhibitor of the soluble guanylyl cyclase (ODQ, 50 μM) were used. We also measured PDE2 and PDE3 mRNA levels in atrial tissue samples from both groups of patients using RT-qPCR. Results We could show that stimulation with CNP increased cGMP levels in human atrial myocytes. However, in myocytes from patients with AF global cGMP responses to CNP and to IBMX was reduced compared to SR. Additionally, there was a difference in response to CNP and IBMX in patients with AF between the right and the left atria. Whereas in the right atria IBMX could further increase cGMP levels in the cell, in the left atria leaded to a reduction in cGMP levels. RT-qPCR showed a tendency of PDE3 to be reduced in AF. On the other hand, PDE2A gene expression was upregulated in the left atria. Conclusions We have shown that PDEs contributes cGMP signaling in the human atria and that they are involved in atrial pathophysiology. Now our data clearly show differences in cGMP regulation in cardiomyocytes isolated from left and right atrium from patients in atrial fibrillation and sinus rhythm. We observe a major role of PDEs, regulating cGMP pathway promoted by the reduced responses in AF, especially PDE2 in the left atria.

Properties of human atrial ICa at physiological temperatures and relevance to action potential

1997 ◽  
Vol 272 (1) ◽  
pp. H227-H235 ◽  
Author(s):  
G. R. Li ◽  
S. Nattel
Keyword(s):  
Action Potential ◽  
Human Atrium ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Maximum Current Density ◽  
Rate Dependent ◽  
Atrial Cells ◽  
Maximum Current ◽  
Reduced Rate

There are no published characterizations of Ca2+ current (ICa) at physiological temperatures in human atrium. Depolarization of human atrial myocytes at 36 degrees C elicited ICa that peaked at +10 mV, with a mean maximum current density of 10.8 +/- 1.1 pA/pF and no evidence for T-type current. Overlap between activation and inactivation curves and incomplete inactivation during pulses comparable to normal action potential duration (APD) were compatible with the observed role of ICa in maintaining the plateau. ICa was frequency dependent between 0.1 and 2 Hz and ICa blockade with 0.2 mM Cd2+ reduced rate-dependent changes in APD: under control, APD at 90% repolarization was 230 +/- 15 ms at 0.1 Hz and 178 +/- 14 ms at 2 Hz (decrease of 52 +/- 5 ms); with Cd2+, values were 121 +/- 7 ms at 0.1 H2 and 115 +/- 6 ms at 2 Hz (decrease of 6 +/- 3 ms, P < 0.01) Isoproterenol (1 microM) increased ICa and prolonged APD from 138 +/- 13 to 199 +/- 15 ms (P < 0.01). These results indicate that, in human atrial cells at 36 degrees C, the properties of L-type ICa contribute importantly to the rate-dependent and autonomic control of APD.

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