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Background. The purpose of the study was to explore the role of the renin-angiotensin system in the disturbance of renal excretory function in the dynamics of alloxan-induced experimental diabetes mellitus. Materials and methods. The experiments were carried out on 78 white non-linear mature male rats with 11-, 26- and 46-day long experimental diabetes mellitus caused by intraperitoneal administration of alloxan (160 mg/kg), against the background of pharmacological blockade of intrarenal renin-angiotensin system, induced by intraperitoneal administration of сaptopril (10 mg/kg). The study of excretory function of the kidneys was provided by the clearance method under the condition of induced water 2-hour diuresis to determine the clearance of endogenous creatinine, glomerular filtration rate, relative water reabsorption, protein content in urine, its excretion. Results. Analysis of changes in renal function after pharmacological blockade of the renin-angiotensin system in rats on day 11 of alloxan diabetes showed a significant increase in diuresis, glomerular filtration rate, endogenous creatinine concentration index, and protein excretion. The pharmacological blockade of the renin-angiotensin system had practically no effect on the intensity of the relative reabsorption of water in alloxan-diabetic rats. On day 26 of alloxan diabetes after captopril administration, there was a slight decrease in final urine volume, glomerular filtration rate, relative water reabsorption, and endogenous creatinine concentration index. At the same time, captopril did not cause an antiproteinuric effect, and protein excretion even demonstrated a tendency to increase. On day 46 of alloxan-induced diabetes after administration of captopril, there was a significant reduction in diuresis, endogenous creatinine clearance and glomerular filtration rate of rats, as well as in urinary protein concentration and excretion. Conclusions. The results of the study allow us to conclude that the initial stage of renal disorders formation in alloxan-induced experimental diabetes is associated with hemodynamic-hyperperfusion nature of renal functioning with preserved renal functional reserve and the structure of the glomerular-tubular apparatus of the kidney, autoregulatory mechanisms. Mentioned compensatory-functional changes in renal function are gradually complicated by an exhaustion of renal functional reserve and pathological activation of intrarenal renin-angiotensin system with subsequent progression of hyperperfusion-ischemic kidney damage, a decrease in the number of functioning nephrons.
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