scholarly journals Annihilation of the pacemaking activity in the sinoatrial node cell and tissue

AIP Advances ◽  
2018 ◽  
Vol 8 (12) ◽  
pp. 125319 ◽  
Author(s):  
Keming Li ◽  
Zhikun Chu ◽  
Xiaodong Huang
Author(s):  
D.G. Tsalikakis ◽  
H.G. Zhang ◽  
D.I. Fotiadis ◽  
G.P. Kremmydas

2016 ◽  
Vol 2 (3) ◽  
pp. 035006 ◽  
Author(s):  
A Pohl ◽  
A Wachter ◽  
N Hatam ◽  
S Leonhardt

2008 ◽  
Vol 105 (40) ◽  
pp. 15617-15622 ◽  
Author(s):  
Solena Le Scouarnec ◽  
Naina Bhasin ◽  
Claude Vieyres ◽  
Thomas J. Hund ◽  
Shane R. Cunha ◽  
...  

The identification of nearly a dozen ion channel genes involved in the genesis of human atrial and ventricular arrhythmias has been critical for the diagnosis and treatment of fatal cardiovascular diseases. In contrast, very little is known about the genetic and molecular mechanisms underlying human sinus node dysfunction (SND). Here, we report a genetic and molecular mechanism for human SND. We mapped two families with highly penetrant and severe SND to the human ANK2 (ankyrin-B/AnkB) locus. Mice heterozygous for AnkB phenocopy human SND displayed severe bradycardia and rate variability. AnkB is essential for normal membrane organization of sinoatrial node cell channels and transporters, and AnkB is required for physiological cardiac pacing. Finally, dysfunction in AnkB-based trafficking pathways causes abnormal sinoatrial node (SAN) electrical activity and SND. Together, our findings associate abnormal channel targeting with human SND and highlight the critical role of local membrane organization for sinoatrial node excitability.


2011 ◽  
Vol 83 (6) ◽  
Author(s):  
Xiaodong Huang ◽  
Yuanyuan Mi ◽  
Yu Qian ◽  
Gang Hu

1994 ◽  
Vol 266 (3) ◽  
pp. C832-C852 ◽  
Author(s):  
S. S. Demir ◽  
J. W. Clark ◽  
C. R. Murphey ◽  
W. R. Giles

A mathematical model for the electrophysiological responses of a rabbit sinoatrial node cell that is based on whole cell recordings from enzymatically isolated single pacemaker cells at 37 degrees C has been developed. The ion channels, Na(+)-K+ and Ca2+ pumps, and Na(+)-Ca2+ exchanger in the surface membrane (sarcolemma) are described using equations for these known currents in mammalian pacemaker cells. The extracellular environment is treated as a diffusion-limited space, and the myoplasm contains Ca(2+)-binding proteins (calmodulin and troponin). Original features of this model include 1) new equations for the hyperpolarization-activated inward current, 2) assessment of the role of the transient-type Ca2+ current during pacemaker depolarization, 3) inclusion of an Na+ current based on recent experimental data, and 4) demonstration of the possible influence of pump and exchanger currents and background currents on the pacemaker rate. This model provides acceptable fits to voltage-clamp and action potential data and can be used to seek biophysically based explanations of the electrophysiological activity in the rabbit sinoatrial node cell.


1981 ◽  
Vol 31 (4) ◽  
pp. 491-500 ◽  
Author(s):  
Akinori NOMA ◽  
Hiroshi KOTAKE ◽  
Shinichiro KOKUBUN ◽  
Hiroshi IRISAWA

1984 ◽  
Vol 55 (2) ◽  
pp. 253-260 ◽  
Author(s):  
W J Marvin ◽  
V L Chittick ◽  
J K Rosenthal ◽  
A Sandra ◽  
D L Atkins ◽  
...  

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