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

ABSTRACT: 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⁺/Ca

SUBMITTER: Morotti S 

PROVIDER: S-EPMC8198068 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature