Chipko T. The influence of blockade AT1-receptors by lozartane on renal function at experimental heart failure.

. In the experiments using 247 rats the animals with dosage-dependent narrowing of abdominal aorta showed the speed slowdown of glomerular filtration (SGF) with development of hypercreatinemia as a result of tubulo-glomerular feedback activation (TGF) and reduction of proximal ion reabsorbtion suppressing the renal acid secretion. The lozartane positive effect of renal fuction has been demonstrated to be realized by TGF blocking. Narrowing of posterior cava vein within 2 months did not exert any negative influence on renal function, however TGF suppression by lozartane led to irrepressible losses of natrium with urina, hyponatriemia, dysfunction of natrium-dependent mechanisms of urine acidification and speed slowdown of glomerular filtration at the background of excess intensification of lipid peroxide oxidation (POL) proteins and proteolysis, as well as a significant tapering of enzymatic counter-radical potential and fibrinolysis in the cortical renal tissue. The parallel narrowing of abdominal aorta and posterior cava vein disturbed the excretory renal activity resulting in the reduction and reinforcement of proximal and distal natrium ion reabsorbtion, respectively, together with suppression of hydro-natrium counter-transport. Lozartane has been found to restore SGF however causing the dysfunction of tubulo-tubular balance and leading to hyponatremia and intensity cut down of natrium-dependent mechanisms of urine acidification. The processes of excessive formation of oxygen radicals in the cortical renal tissue have been shown to the basic factor of renal status dysfunction in cases of heart failure. These processes caused POL and protein upsurge, activated proteolysis and reduced the intensity of enzymatic fibrinolysis.