Measurement of Ca2+-release-dependent inward current reveals two distinct components of Ca2+ release from sarcoplasmic reticulum in guinea-pig atrial myocytes

1991 ◽  
Vol 417 (6) ◽  
pp. 638-644 ◽  
Author(s):  
T. Budde ◽  
P. Lipp ◽  
L. Pott
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Atrial Myocytes ◽  
Inward Current

Modulation of action potential by [Ca2+]i in modeled rat atrial and guinea pig ventricular myocytes

2002 ◽  
Vol 282 (3) ◽  
pp. H1047-H1054 ◽  
Author(s):  
Chunlei Han ◽  
Pasi Tavi ◽  
Matti Weckström
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Action Potential ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Transient Increase ◽  
Current Increase ◽  
Inward Current ◽  
Gp Model ◽  
Long Action

We simulated mechanisms that increase Ca2+ transients with two models: the Luo-Rudy II model for guinea pig (GP) ventricle (GP model) representing long action potential (AP) myocytes and the rat atrial (RA) model exemplifying myocytes with short APs. The interventions were activation of stretch-gated cationic channels, increase of intracellular Na+ concentration ([Na+]i), simulated β-adrenoceptor stimulation, and Ca2+accumulation into the sarcoplasmic reticulum (SR). In the RA model, interventions caused an increase of AP duration. In the GP model, AP duration decreased except in the simulated β-stimulation where it lengthened APs as in the RA model. We conclude that the changes in the APs are significantly contributed by the increase of the Ca2+ transient itself. The AP duration is controlled differently in cardiac myocytes with short and long AP durations. With short APs, an increase of the Ca2+ transient promotes an inward current via Na+/Ca2+-exchanger lengthening the AP. This effect is similar regardless of the mechanism causing the increase of the Ca2+ transient. With long APs the Ca2+ transient increase decreases the AP duration via inactivation of the L-type Ca2+ current. However, L-type current increase (as with β-stimulation) increases the AP duration despite the simultaneous Ca2+ transient augmentation. The results explain the dispersion of AP changes in myocytes with short and long APs during interventions increasing the Ca2+transients.

Intracellular citrate induces regenerative calcium release from sarcoplasmic reticulum in guinea-pig atrial myocytes

1995 ◽  
Vol 429 (6) ◽  
pp. 797-804 ◽  
Author(s):  
G. Callewaert ◽  
K. R. Sipido ◽  
E. Carmeliet ◽  
L. Pott ◽  
P. Lipp
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Calcium Release ◽  
Atrial Myocytes

Mechanism of current-induced early afterdepolarizations in guinea pig ventricular myocytes

1994 ◽  
Vol 267 (4) ◽  
pp. H1419-H1428 ◽  
Author(s):  
Z. Ming ◽  
R. Aronson ◽  
C. Nordin
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Threshold Current ◽  
Constant Current ◽  
Delayed Rectifier ◽  
Control Solution ◽  
Early Afterdepolarizations ◽  
Inward Current ◽  
Channel Current

We investigated possible ionic mechanisms that cause early afterdepolarizations (EADs) following the injection of constant inward current in guinea pig ventricular myocytes by several interventions that affect failure of action potential repolarization. The amount of constant current was adjusted to measure the threshold potential (Vth) associated with the minimum inward current required for inducing EADs [threshold current (Ith)] and also the magnitude of EADs at Vth and following adjustment of current to generate takeoff potentials of -30 and -20 mV. Interventions associated with either inhibition of Ca2+ release from the sarcoplasmic reticulum (ryanodine 5 x 10(-6) M) or L-type membrane Ca2+ channel current (verapamil 1.1 x 10(-5) M and nisoldipine 5 x 10(-7) M) reduced or abolished EADs arising from -30 or -20 mV. Cells that generated delayed afterdepolarizations (DADs) in the absence of depolarizing current after 20 stimulations at 5 Hz either in control solution or following interventions associated with Ca2+ loading (reduced extracellular [K+] or increased extracellular [Ca2+]) also developed a marked shift in Vth of current-induced EADs at 1-Hz stimulation to more negative potentials [60.3 +/- 10.7 mV (mean +/- SD, n = 17) vs. -41.7 +/- 6.4 mV in cells without DADs in control solution (n = 25), P < 0.001]. Ca2+ loading also increased the magnitude of EADs arising from Vth and -20 mV. Exposure to quinidine (1.23 x 10(-5) M), which blocks both Na+ and delayed rectifier K+ channels, significantly reduced Ith but had only minimal effect on the magnitude of EADs. Our results suggest that L-type Ca2+ channel current and [Ca2+]-sensitive inward current associated with release of Ca2+ from the sarcoplasmic reticulum are the major currents that cause this form of EADs, and that Ca2+ loading promotes the development of large EADs likely to propagate to normal tissue.

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

scholarly journals Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2 + ATPase in atrial myocytes

2009 ◽  
Vol 10 (3) ◽  
pp. 121-126 ◽  
Author(s):  
Cho-Kai Wu ◽  
Chuen-Den Tseng ◽  
Yin-Tsen Huang ◽  
Chia-Shan Hsieh ◽  
Wei-Shan Tsai ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sarcoplasmic Reticulum ◽  
Atrial Myocytes
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