Na+ current in human atrial myofibroblasts alters myocyte excitability: A computational study

摘要

Previous studies have shown that human atrial myofibroblasts can express a Na+ current (Ina_myofb). This preliminary study aimed to identify the role of INa_myofb integrated in electrotonic myofibroblast-myocyte (myofb-m) coupling on the excitability and repolarization of myocyte and myofibroblast. Mathematical modeling was done using a combination of (1) the Maleckar et al. model of the human atrial myocyte, (2) the MacCannell et al. “active” model of the human cardiac myofibroblast, and (3) our formulation of Ina_myofb based upon experimental findings from Chatelier et al. The results showed that (1) for myocytes, the addition of INa_myofb decreased the reductions of the peak of action potential (Vmax) and action potential duration (APD), and increased the degree of resting membrane potential (Vrest) depolarization as compared to no INa_myofb integrated in myofb-m coupling. (2) for myofibroblasts, more significant electrotonic depolarizations were exhibited with addition of INa_myofb. INa_myofb should be considered in future pathological cardiac mathematical modeling, such as atrial fibrillation and cardiac fibrosis.