Spinal cord injury represents a complex and serious medical condition characterized by damage to the spinal cord, causing profound functional impairment. The consequences of such an injury may include paralysis, loss of sensation, and disruptions in vital bodily functions, such as bladder and bowel control. The renin-angiotensin system, predominantly acting through the AT1 receptor, regulates blood pressure and hydro-electrolytic balance. However, the AT2 receptor (AT2R) also plays a crucial role, especially in processes related to neuroregeneration. In the present study, the AT2R was stimulated in an experimental model of severe spinal cord compression in adult Wistar rats. The selective AT2R agonist CGP42112 was systematically administered by osmotic minipumps (s.c.) from the 14th to the 28th day post-injury. RT-PCR and Western blot analysis revealed increased expression of axonal and myelin markers, including neurofilaments, myelin basic protein, and CNPase. Additionally, the marker of axonal regeneration (GAP43) exhibited increased expression after AT2R stimulation compared to control specimens. Histological staining confirmed a statistically significant amount of spared spinal cord tissue, coupled with reduced microcyst and cystic cavity formation, particularly in caudal regions. Of note, motor function recovery was markedly faster after AT2R stimulation than in spinal cord injury alone (BBB locomotor score: 10.4 points vs. 9 points). A number of these favourable effects were partially or entirely prevented by the blockade of the AT2 receptor with specific antagonist. In conclusion, these findings indicate that the strategy to stimulate AT2 receptor holds promise as a therapeutic intervention for spinal cord injuries. Supported by APVV-22-0248,VEGA 2/0123/23.