Abstract: As a resistant hypertension, the pathogenesis of salt-sensitive hypertension is complex. Although mineralocorticoid receptor activation and renal injury play a key role in the development of salt-sensitive hypertension, the specific pathological mechanism is currently unclear. In this study, a model of Dahl SS hypertension was established by high-salt diet induction to explore the pathological mechanism of salt-sensitive hypertension and kidney injury. Compared with salt-insensitive SS-¹³BN rats, long-term high-salt diet caused local activation of sympathetic nerves and renin-angiotensin-aldosterone system (RAAS) in the kidney of Dahl SS rats, which eventually activated mineralocorticoid receptors (MR), resulting in increased expression of epithelial sodium channels (ENaC), enhanced inflammatory response and oxidative stress, renal fibrosis, and triggered increased expression of phosphorylated actin (P-Cofilin) and podocin in the kidney, resulting in podocyte damage and ultimately renal injury and hypertension.