scholarly journals Functional coupling between glycolysis and excitation—contraction coupling underlies alternans in cat heart cells

2000 ◽  
Vol 524 (3) ◽  
pp. 795-806 ◽  
Author(s):  
Jörg Hüser ◽  
Yong Gao Wang ◽  
Katherine A. Sheehan ◽  
Fredy Cifuentes ◽  
Stephen L. Lipsius ◽  
...  
Keyword(s):  
Functional Coupling ◽  
Heart Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cat Heart

Inhibition by cocaine of excitation-contraction coupling in isolated cardiomyocytes

1991 ◽  
Vol 260 (1) ◽  
pp. H50-H57 ◽  
Author(s):  
G. Stewart ◽  
E. Rubin ◽  
A. P. Thomas
Keyword(s):  
Cell Damage ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Electrical Stimulus ◽  
Ratio Method ◽  
Heart Cells ◽  
Excitation Light ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rat Heart Cells

The effects of cocaine on the Ca2+ fluxes responsible for excitation-contraction coupling were studied in isolated ventricular rat heart cells loaded with the fluorescent Ca2+ indicator fura-2. Ca2+ transients in response to electrical field stimulation were followed using a fluorescence ratio method in which excitation light was alternated with 5-ms resolution. The cardiomyocytes maintained a basal cytosolic Ca2+ concentration of approximately 70 nM, which increased to a peak of 450 nM in response to each electrical stimulus. The addition of cocaine (10 microM) to cells stimulated at 0.4 Hz decreased the magnitude of the electrically induced Ca2+ transients by 30 +/- 4% within 5 s. This inhibitory effect of cocaine was dose dependent, with a 50% reduction in the Ca2+ transient occurring at 40 microM cocaine. The effects of cocaine were not associated with any permanent cell damage and could be reversed by washing the cells free of the drug. Cytosolic Ca2+ increases in response to K(+)-induced depolarization of the cardiomyocytes were much less sensitive to cocaine than the electrically induced Ca2+ transients. In this respect the effects of cocaine were similar to the actions of lidocaine and tetrodotoxin but distinct from the effects of nitrendipine and verapamil. Cocaine had no effect on the caffeine-releasable Ca2+ pool in cardiomyocytes. These data demonstrate that cocaine directly inhibits the Ca2(+)-dependent steps of excitation-contraction coupling in heart muscle cells. Sarcolemmal Na+ channels represent a possible locus for this action of cocaine.

scholarly journals The IQ Motif is Crucial for Cav1.1 Function

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Katarina Stroffekova
Keyword(s):  
Skeletal Muscle ◽  
High Voltage ◽  
Functional Coupling ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Whole Cell ◽  
Iq Motif ◽  
Contraction Coupling

Ca2+-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca2+channels. The skeletal muscle Cav1.1 also exhibits Ca2+-/CaM-dependent modulation. Here, whole-cell Ca2+current, Ca2+transient, and maximal, immobilization-resistant charge movement(Qmax)recordings were obtained from cultured mouse myotubes, to test a role of IQ motif in function of Cav1.1. The effect of introducing mutation (IQ to AA) of IQ motif into Cav1.1 was examined. In dysgenic myotubes expressing YFP-Cav1.1AA, neither Ca2+currents nor evoked Ca2+transients were detectable. The loss of Ca2+current and excitation-contraction coupling did not appear to be a consequence of defective trafficking to the sarcolemma. TheQmaxin dysgenic myotubes expressing YFP-Cav1.1AAwas similar to that of normal myotubes. These findings suggest that the IQ motif of the Cav1.1 may be an unrecognized site of structural and functional coupling between DHPR and RyR.

scholarly journals Dynamics of Calcium Sparks and SR Calcium Leak During Excitation-Contraction Coupling in Mouse Heart Cells

2014 ◽  
Vol 106 (2) ◽  
pp. 320a-321a
Author(s):  
George S.B. Williams ◽  
Andrew P. Wescott ◽  
W.J. Lederer ◽  
M. Saleet Jafri
Keyword(s):  
Mouse Heart ◽  
Heart Cells ◽  
Calcium Sparks ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Sr Calcium Leak

Excitation-Contraction Coupling in Heart Cells.

1990 ◽  
Vol 588 (1 Embryonic Ori) ◽  
pp. 190-206 ◽  
Author(s):  
W. J. LEDERER ◽  
J. R. BERLIN ◽  
N. M. COHEN ◽  
R. W. HADLEY ◽  
D. M. BERS ◽  
...  
Keyword(s):  
Heart Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

Implication of the nucleus in excitation contraction coupling of heart cells

1996 ◽  
Vol 154 (2) ◽  
pp. 113-121 ◽  
Author(s):  
Ghassan Bkaily ◽  
Nadine Gros-Louis ◽  
Radha Naik ◽  
Doris Jaalouk ◽  
Pierre Pothier
Keyword(s):  
Heart Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

scholarly journals Local control of excitation-contraction coupling in rat heart cells.

1994 ◽  
Vol 474 (3) ◽  
pp. 463-471 ◽  
Author(s):  
W G Wier ◽  
T M Egan ◽  
J R López-López ◽  
C W Balke
Keyword(s):  
Local Control ◽  
Rat Heart ◽  
Heart Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rat Heart Cells

scholarly journals Excitation Contraction Coupling in Hypertrophy and Failing Heart Cells

2021 ◽  
Vol 271 ◽  
pp. 03008
Author(s):  
Yiqiu Zhou
Keyword(s):  
Heart Failure ◽  
Calcium Release ◽  
Heart Diseases ◽  
Calcium Handling ◽  
Heart Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Failing Heart ◽  
Failure Models ◽  
And Function

The contraction of the heart is dependent on a process named the excitation-contraction coupling (E-C coupling). In hypertrophy and failing heart models, the expression, phosphorylation and function of key calcium handling proteins involved in E-C coupling are altered. It’s important to figure out the relationship changes between calcium channel activity and calcium release from sarcoplasmic reticulum (SR). This review will therefore focus on novel components of E-C coupling dysfunction in hypertrophy and failing heart, such as L-type Ca2+ channel (LCC), ryanodine receptor type-2 channel (RyR2) and SR Ca ATPase (SERCA), and how these molecular modifications altered excitation-contraction coupling. A lot of literature was well read and sorted. Recent findings in E-C coupling during hypertrophy and heart failure were focused on. Most importantly, the electrophysiological and signal pathway data was carefully analyzed. This review summarizes key principles and highlights novel aspects of E-C coupling changes during hypertrophy and heart failure models. Although LCC activity changed little, the loss of notch in action potential, reduced Ca2+ transient amplitude and desynchronized Ca2+ sparks resulted in a decreased contraction strength in hypertrophy and heart failure models. What’s more, L-type Ca2+ current becomes ineffective in triggering RyR2 Ca2+ release from SR and the SR uptake is reduced in some models. It has great meanings in understanding the E-C coupling changes during different heart diseases. Theses novel changes suggest potential therapeutic approaches for certain types of hypertrophy and heart failure.

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