Abstract: Primary aldosteronism (PA) is a major cause of secondary hypertension, characterized by complex interactions between ion channel dysfunction and adrenal steroidogenesis. Animal models are essential for elucidating its underlying mechanisms. This review provides a mechanism-oriented synthesis of commonly used PA models, comparing genetically modified and functional models in terms of their roles in the “membrane depolarization-calcium signaling-CYP11B2 activation” axis and their ability to recapitulate human phenotypes. Overall, genetic models are useful in dissecting molecular mechanisms, whereas functional models more closely mimic sustained aldosterone excess observed in clinical settings. However, current models remain limited by insufficient organ specificity and phenotypic consistency. Future efforts should focus on integrative and stratified model application, combined with emerging multi-omics approaches to advance mechanistic insights and improve translational applicability in PA.