Objective. To evaluate the association of NOS3 and ESR1 polymorphisms with the functional state of the endothelial system, angiogenesis regulation and sex steroid reception in girls with puberty abnormal uterine bleeding (AUBP). Material and methods. The study consisted of 96 adolescent girls with AUBP. 32 girls were born with intrauterine growth retardation (IUGR) and 37 girls were born with normal weight. The control group consisted of 27 healthy girls. Gene polymorphisms NOS3 786 T>C, 894 G>T and ESR1 351 A>G and 397 T>C were studied by PCR real time method. Indicators of the endothelial function and angiogenesis regulation were assessed by enzyme immunoassay in accordance with the recommendations of the kits manufacturers. The level of sex steroids receptors in the vaginal mucosa was investigated by immunocytochemistry. Results. Girls with uterine bleeding, born with IUGR, had higher rate of polymorphic allele C NOS3 gene 786 T>C (for homozygotes OR=2.03; CI 95% 1.12-3.68; p=0.04; for heterozygotes OR=1.68; 95% CI 1.09-2.60; p=0.046) and genotype Pvull-CC ESR1 (OR=4.58; 95% CI 0.97-21.68; p=0.04). They showed a reduction in the level of endogenous nitric oxide [10.71 (6.89-17.29) umol /ml in the control group - 18.39 (14.58-23.62) umol/ml; p=0.003], endothelin-1 [0.57 (0.42-4.80) fmol/ml vs. 1.34 (0.45-4.74) fmol/ml in the control group; p=0.015] and a three-fold increase in the level of angiogenesis activator - vascular endothelial growth factor (371.75 ng/ml (219.9-565.7), the control 195.05 ng/ml (78.21-301.85); p=0.0017). These girls demonstrated high local level of ERα receptors expression in vaginal mucosa (24.52±4.86 points against 1.06±0.28 points in the control; p<0.0001). Conclusion. Intrauterine endothelial dysfunction may be important factor in abnormal uterine bleeding in girls born with intrauterine growth retardation.