BACKGROUND. Determining the pathogenetic mechanisms of small-caliber renal artery remodeling in chronic glomerulonephritis (GN) is an urgent task of nephrology, the implementation of which will allow establishing new diagnostic and therapeutic approaches to patients management. THE AIM: To evaluate the influence of hemodynamic, tubulointerstitial, and endothe- liotropic risk factors on the probability of remodeling of interlobular arteries in an experimental model of glomerulonephritis. MATERIALS AND METHODS. The experiment included 45 individuals of white mongrel rats, 3 of which were used to prepare an antigen suspension (AS), and 42 rats were divided into 4 groups: 9 individuals in the main groups (with the introduction of only AS, with the introduction of an incomplete Freund adjuvant, with AS and sodium chloride, with AS and perindopril) and 6 ratsin the control group. Glomerulonephritis was formed in the main groups of the experiment. Systolic blood pressure (SAD), the protein level in the urine, and the presence of edematous syndrome were monitored initially, on the 15th, 30th, and 60th day of the experiment. The size of the interlobular artery (MA) was determined by the morphological study, and the expression of VEGF and TGFp in the kidneys. RESULTS. Morphological signs of glomerulonephritis were obtained in all the main groups of the experiment as early as day 15. The greatest increase in SAD, protein in the urine, the presence of edematous syndrome in groups with the introduction of AS and AS with sodium chloride was found. The highest expression of VEGF and TGFp was found in these groups of rats. In the group with AS with perindopril, normotension was formed, the protein level was lower than in rats with AS with or without the use of sodium chloride, and there was no edematous syndrome. The expression of VEGF and TGFp was minimal. Interlobular artery remodeling in established groups of AS an AC with sodium chloride. In the remaining groups of rats, the size of the interlobular arteries was comparable to the control group. CONCLUSION. The leading role of systemic blood pressure in the remodeling of small-diameter kidney arteries in glomerulonephritis has been established. Despite the presence of active glomerulonephritis in rats, the structure of small arteries does not change during the formation of normotension.
