Prenatal hypoxia plays a crucial role in programming long-term cardiovascular dysfunction through mechanisms like endothelial dysfunction and nitric oxide system impairment, highlighting the potential of therapeutic agents, such as thiotriazoline, angiolin, mildronate, and L-arginine, for mitigating these adverse effects. Methods. Levels of sEPCR, Tie2 tyrosine kinase, VEGF-B, SOD1/Cu-Zn SOD, GPX4, and GPX1 were measured in the heart's cytosolic homogenate using ELISA. Results. Modeling prenatal hypoxia (PH) resulted in significant alterations in the concentrations of proteins linked to endothelial function and oxidative stress in the heart cytosol of experimental animals, including an increase in sEPCR and reductions in Tie-2, VEGF-B, Cu/ZnSOD, GPX4, and GPX1 levels. Postnatal administration of nitric oxide modulators (L-arginine, thiotriazoline, angiolin, and mildronate) demonstrated differential efficacy in normalizing these proteins. Notably, angiolin produced the most substantial therapeutic effect, restoring Tie2, VEGF-B, and antioxidant enzyme levels to near-normal levels. Our results highlight the efficacy of Angiolin and Thiotriazoline in restoring endothelial function and antioxidant enzyme levels in the car-diovascular system following prenatal hypoxia, supporting their potential as early postnatal in-terventions to prevent long-term cardiovascular dysfunction.