The role of Ca2+ release from sarcoplasmic reticulum in the regulation of sinoatrial node automaticity

1996 ◽  
Vol 11 (5) ◽  
pp. 234-241 ◽  
Author(s):  
Tadayoshi Hata ◽  
Takeshi Noda ◽  
Masao Nishimura ◽  
Yoshio Watanabe
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Sinoatrial Node ◽  
Sinoatrial Node Automaticity

scholarly journals Role of sarcolemmal ATP-sensitive K+channels in the regulation of sinoatrial node automaticity: an evaluation using Kir6.2-deficient mice

2008 ◽  
Vol 586 (11) ◽  
pp. 2767-2778 ◽  
Author(s):  
Koichi Fukuzaki ◽  
Toshiaki Sato ◽  
Takashi Miki ◽  
Susumu Seino ◽  
Haruaki Nakaya
Keyword(s):  
Sinoatrial Node ◽  
K Channels ◽  
Deficient Mice ◽  
Sinoatrial Node Automaticity

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

scholarly journals The Role of the Calcium and the Voltage Clocks in Sinoatrial Node Dysfunction

2011 ◽  
Vol 52 (2) ◽  
pp. 211 ◽  
Author(s):  
Boyoung Joung ◽  
Peng-Sheng Chen ◽  
Shien-Fong Lin
Keyword(s):  
Sinoatrial Node ◽  
Sinoatrial Node Dysfunction
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