Aim of the study. To assess the degree of endothelial dysfunction and renal function in experimental ischemic stroke (EIS) in rats on the dynamics of pharmacotherapy. Materials and Methods. The subject of experimental studies were 105 adult mongrel white male rats. The object of the study were the serum and urine of rats. The model of cerebral circulation reproduced by temporary clipping of the left common carotid artery. The controls were 20 intact animals. Results. The results indicate to the development of endothelial dysfunction with EIS with the activation of neoangiogenesis in experimental animals. Pharmacotherapy with suksinasol for 7 days caused reduction of the level of ET-1 with respect to the values of untreated animal group and was still significantly higher than control group of rats in 2.5 times. At the same time, the level of VEGF A (vascular endothelial growth factor A) significantly decreased respectively to untreated group of rats in 1.65 times (p<0.01), but was still higher than control values in 1.74 times (p<0.01). Development of proteinuria, microalbuminuria and creatininuria in rats with EIS apparently was due to the development of hemodynamic changes in the kidney and glomerular basal membrane permeability, and due to the enhanced excretion of toxins and protein degradation products. Conclusion. The endothelial and renal dysfunctions with activation of neoangiogenesis develop on the model of EIS. Pharmacotherapy corrects the identified changes to some extent. Tivortin and choline alfoscerate were more effective, possibly, because of decrease of hemodynamic disturbances and neurotrophic effects.