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

Evidence for presence of Ca2+ channel-gated Ca2+ stores in neonatal human atrial myocytes

1995 ◽  
Vol 268 (3) ◽  
pp. H1195-H1201 ◽  
Author(s):  
S. N. Hatem ◽  
T. Sweeten ◽  
V. Vetter ◽  
M. Morad
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Voltage Dependence ◽  
Atrial Myocytes ◽  
Old Patients ◽  
Whole Cell ◽  
Human Atrial Myocytes ◽  
Fura 2 ◽  
Primary Mechanism ◽  
Human Atrial Appendages

The characteristics of Ca2+ signaling in fura 2-loaded whole cell-clamped myocytes obtained from samples of human atrial appendages of 3-day to 4-yr-old patients were examined. In isolated myocytes, activation of Ca2+ current (ICa) (2.47 +/- 0.23 pA/pF) at 0 mV elicited sizable intracellular Ca2+ (Cai) transients (240 +/- 45 nM), which were caused by the release of Ca2+ from intracellular stores as they were suppressed in the presence of ryanodine or caffeine. The voltage dependence of both Cai transients and ICa were similar and bell shaped. The rate of release of Ca2+, normalized for the maximal Ca2+ release, increased with age, indicating increased efficiency of Ca2+ signaling in more mature myocytes. The results suggest that ICa-gated release of Ca2+ from the sarcoplasmic reticulum is the primary mechanism regulating the signaling of contraction in early postnatal as well as older human atrial myocytes.

Different Compartments of Sarcoplasmic Reticulum Participate in the Excitation-Contraction Coupling Process in Human Atrial Myocytes

1997 ◽  
Vol 80 (3) ◽  
pp. 345-353 ◽  
Author(s):  
Stephane N. Hatem ◽  
Agnes Benardeau ◽  
Catherine Rucker-Martin ◽  
Isabelle Marty ◽  
Patricia de Chamisso ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atrial Myocytes ◽  
Excitation Contraction Coupling ◽  
Human Atrial Myocytes ◽  
Coupling Process ◽  
Contraction Coupling

scholarly journals Atrial Fibrillation Is Associated With Increased Spontaneous Calcium Release From the Sarcoplasmic Reticulum in Human Atrial Myocytes

Circulation ◽  
2004 ◽  
Vol 110 (11) ◽  
pp. 1358-1363 ◽  
Author(s):  
Leif Hove-Madsen ◽  
Anna Llach ◽  
Antoni Bayes-Genís ◽  
Santiago Roura ◽  
Enrique Rodriguez Font ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes

Acetylcholine-sensitive potassium channels in human atrial myocytes

1990 ◽  
Vol 259 (6) ◽  
pp. H1730-H1735 ◽  
Author(s):  
R. Sato ◽  
I. Hisatome ◽  
J. A. Wasserstrom ◽  
C. E. Arentzen ◽  
D. H. Singer
Keyword(s):  
Single Channel ◽  
K Channel ◽  
Channel Activity ◽  
Atrial Myocytes ◽  
Open Probability ◽  
Human Atrial Myocytes ◽  
Open Time ◽  
Patch Pipette ◽  
Single Channel Activity ◽  
Gamma S

Single channel recording techniques were used to study acetylcholine (ACh)-sensitive K+ channel activity in human atrial myocytes isolated from specimens obtained during corrective cardiac surgery. Under conditions of cell-attached patch, the presence of ACh in the patch pipette activated K+ channels. Single channel activity occurred in periodic bursts. The channels exhibited a slope conductance of 46 +/- 2 pS inwardly (means +/- SD, n = 4). During a burst, both open and closed time histograms were fitted by a single exponential curve, suggesting the existence of one open and one closed state during a burst. Open probability increased directly with ACh concentration without affecting open time. The channel could be activated by GTP and guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) (in the presence and absence of ACh in the pipette, respectively). Slope conductance, the response to GTP and GTP gamma S, and the independence of activation from Ca2+ were similar to those for other species. In contrast, sensitivity to ACh appeared diminished compared with frog atrial myocytes.

Src family tyrosine kinases inhibit single L-type: Ca2+channel activity in human atrial myocytes

2004 ◽  
Vol 37 (3) ◽  
pp. 735-745 ◽  
Author(s):  
Frank Schröder ◽  
Gunnar Klein ◽  
Tanja Frank ◽  
Michaela Bastein ◽  
Sylvio Indris ◽  
...  
Keyword(s):  
Tyrosine Kinases ◽  
Channel Activity ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Src Family Tyrosine Kinases

Mechanisms of inactivation of L-type calcium channels in human atrial myocytes

1997 ◽  
Vol 272 (4) ◽  
pp. H1625-H1635 ◽  
Author(s):  
H. Sun ◽  
N. Leblanc ◽  
S. Nattel
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Time Course ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Whole Cell Patch Clamp ◽  
Dependent Inactivation ◽  
Rapid Inactivation ◽  
Voltage Dependent ◽  
Ca2 Channels

We used whole cell patch-clamp and microfluorimetric (indo 1) techniques to measure Ca2+ current through L-type Ca2+ channels (I(Ca)) and Ca2+ transients in human atrial myocytes. During 1-s depolarizing pulses, I(Ca) inactivation was biexponential. The rate of rapid inactivation was slowed by ryanodine and was correlated with the rate of rise of cytoplasmic free Ca2+ concentration (r = 0.80, P < 0.01). Slower-phase I(Ca) inactivation was not affected by ryanodine but was accelerated by increasing the availability of Ca2+ to permeate the Ca2+ channel. Thus Ca2+ released from the sarcoplasmic reticulum (SR) was responsible for most I(Ca) inactivation during the first 50 ms of a depolarization to 0 mV, and thereafter inactivation by Ca2+ permeating the channel predominated. Pure voltage-dependent inactivation had a much slower time course of development (tau > 2 s) and played a smaller role than Ca2+-dependent mechanisms over a duration comparable to that of an action potential. We conclude that human atrial myocytes show both voltage- and Ca2+-dependent I(Ca) inactivation, that Ca2+-dependent mechanisms predominate over the time course of an action potential, and that although both Ca2+ released from the SR and Ca2+ permeating Ca2+ channels play a role, SR-released Ca2+ is particularly important in early, rapid I(Ca) inactivation, whereas Ca2+ permeating Ca2+ channels is more important in the slower phase of Ca2+-dependent inactivation.

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