NEPHROPROTECTIVE EFFECT OF BLOCKADE OF AT₁ RECEPTORS AFTER ACUTE DEGRADATION OF URODYNAMICS

Abstract

THE AIM of the investigation is concrete definition of morphogenetic mechanisms of realization of nephroprotective effect of AT₁ receptor blockade in rats after degradation of urodynamics which was produced in the model of acute obstruction of the ureter. MATERIAL AND METHODS. The first group (n=30) included animals without pharmacological correction. Rats of the second group (n=30) were given Lozartan (10 mg/kg a day) during 2 weeks after restoration of urodynamics. The morphological state of the kidney was investigated in 7, 14 and 30 days using quantitative criteria. RESULTS. In 7 days in the second group of animals there was optimization of the glomerular and peritubular blood flow with the decreased degree of alteration of the tubules of the cortical and external medullary substance by 26.41% and 48.51% respectively. The specific volume (SV) of infiltrates in the cortex external and internal medulla of the kidney with AT₁ receptor blockade was respectively 36.57%, 40.34% (p<0.01 and 17.42% lower (p<0.05) that in the first group. Within 14 days in the cortical and external medullary substance of the postobstructive kidneyof the 2 group rats there was decreased intensity of the inflammatory infiltration, normalization of the state of peritubular capillaries, intensification of the reparative processes in the kidney: SV of the tubules with normal structure and regeneration signs was 9.67% (p<0.05) and 59.26% (p<0.01) higher, and SV of the tubules with the signs of alteration – 60.19% lower that in the first group (p< 0.01). By the 30th day restriction of fibrosing in the postobstructive kidney was revealed: the interstitium SV was 21.43%, 25.53% and 17.65% lower than in the first group respectively in the cortical, external and internal medullary substance. CONCLUSION. AT₁ receptor blockade facilitates the restortation of the structural-fuctional state of the cortical substance, completion of the inflammatory-reparative process and limitation of fibrosis in the medullary substance of the postobstructive kidney.