Vasopressin (AVP) plays an important role in concentration of urine and water balance maintance. It inhances solute-free water reabsorption stimulating V2-receptors in collecting tubule and sodium excretion via V1a-receptors in distal nephron. V2-receptors were found in distal nephron. The aim of the study was to investigate the role of renal V2-receptors in regulation of sodium excretion. The experiments were carried out using Wistar rats. Treatment of the animals was performed in accordance with Russian and EU guidelines on the use of animals in research. Protocols were approved by the Ethical Committee of the Institute. We applied antagonist of V2-receptors (Bachem, Bubendorf, Switzerland) 15 or 50 nmol/kg and sodium load consisting in intraperitoneal administration of 18 ml/kg of 2.5% NaCl intraperitoneally. AVP concentrations were quantified using a commercially available enzyme immunoassay kit (Enzo Life Sciences, Inc., Farmingdale, NY, USA). Diuresis was recorded as spontaneous urination. Osmolality (Micro-Osmometer 3300, Advanced Instruments, USA) and sodium concentration in urine (Sherwood-420 flame photometer, Sherwood Scientific, Cambridge) was measured in each sample. Results were normalized per 100 g bw and presented as M±m. All measurements between groups were compared by t-test with Bonferroni correction, p < 0.05 was considered significant. Compared to vehicle the injection of V2-antagonist increased renal solute excretion (246±8 vs. 454±31 µOsm/2 h, p<0.05), renal sodium excretion (7±2 vs. 37±9 µmol/2 h, p<0.05), solute-free water clearance (CH2O) (-0.40±0.05 vs. 1.76±0.26 ml (p<0.05) and 17-fold increase of renal AVP excretion was observed. The blockade of V2-receptors led to severe water loss what caused AVP secretion and natriuresis consequently. After sodium load the urine solute and sodium excretion rised to 849±42 µOsm/2 h and to 236±15 µmol/2 h (p<0.05), but CH2O decreased to -2.4±0.14 ml/2 h (p<0.05). The injection of 50 nmol/kg of V2-antagonist following sodium load inhanced renal solute excretion to 1437±25 µOsmol/2 h and sodium excretion to 428±25 µmol/2 h (p<0.05), and reduced CH2O to -0.65±0.16 ml/2 h (p<0.05). AVP takes part in renal sodium excretion regulation due to stimulation of both subtypes of V-receptors. The main finding of the study is that activation of V2-receptors leads not only to decreased solute-free water clearance, but inhanced urinary sodium reabsorbtion that contributes to increased osmotic gradient in renal medulla necessary for maximal water conservation. The work was supported by the government budget funds for state assignment for 2013-2017 (N 01201351572).