Mathematical action potential (AP) modeling is a well-established but still-developing area of research to better understand physiological and pathological processes. In particular, changes in AP mechanisms in the isoproterenol (ISO) -induced hypertrophic heart model are incompletely understood. Here we present a mathematical model of the rat AP based on recordings from rat ventricular myocytes. In our model, for the first time, all channel kinetics are defined with a single type of function that is simple and easy to apply. The model AP and channels dynamics are consistent with the APs recorded from rats for both Control (absence of ISO) and ISO-treated cases. Our mathematical model helps us to understand the reason for the prolongation in AP duration after ISO application while ISO treatment helps us to validate our mathematical model. We reveal that the smaller density and the slower gating kinetics of the transient K⁺ current help explain the prolonged AP duration after ISO treatment and the increasing amplitude of the rapid and the slow inward rectifier currents also contribute to this prolongation alongside the flux in Ca²⁺ currents. ISO induced an increase in the density of the Na⁺ current that can explain the faster upstroke. We believe that AP dynamics from rat ventricular myocytes can be reproduced very well with this mathematical model and that it provides a powerful tool for improved insights into the underlying dynamics of clinically important AP properties such as ISO application.

数学动作电位（AP）建模是一个完善但仍在发展中的研究领域，目的是更好地了解生理和病理过程。尤其是，对异丙肾上腺素（ISO）引起的肥厚性心脏模型中AP机制的变化尚不完全了解。在这里，我们根据大鼠心室肌细胞的记录提出大鼠AP的数学模型。在我们的模型中，所有通道动力学首次使用一种简单且易于应用的函数定义。模型的AP和通道动态与对照（不存在ISO）和ISO治疗的病例从大鼠记录的AP一致。我们的数学模型可以帮助我们了解应用ISO后AP持续时间延长的原因，而ISO处理则可以帮助我们验证数学模型。⁺电流有助于解释ISO处理后AP持续时间的延长以及快速和缓慢的内向整流器电流幅度的增加，以及Ca ²⁺电流的通量，也有助于这种延长。ISO导致Na ⁺电流密度增加，这可以解释更快的中风。我们相信，通过这种数学模型可以很好地重现大鼠心室肌细胞的AP动态，并且它提供了一个强大的工具，可以更好地了解具有临床意义的AP属性（例如ISO应用）的基本动态。