PARADOXICAL EFFECT OF ANGIOTENSIN II RECEPTOR (TYPE 1) BLOCKER, VALSARTAN, ON GENTAMYCIN-INDUCED ACUTE RENAL FAILURE IN RAT.
|Full paper||Not Available|
There are a controversial data about the role of angiotensin II in the pathogenesis of gentamycin induced nephrofoxi city. Also, the role of angiotensin II type 1 receptor ('A Ti) blockers in toxin-induced acute renal failure and the influence of blood pressure reduction induced by this drug need to be evluated Valsartan, (AT)) blocker, in a dose of 3mg/kg/day (which produce minimal effect on arterial blood pressore) and 12mg/kg/day (which produpe significant reduction in arterial blood, pressure) were adminstered orally, fbr 8 days concomitant with gentamycin (100 mg/kg/day Sc). All rats were sacrificed 8 days after siarting experiment. The kidney' function parameters (serum urea and creatinine), histopathblogyical changes, and antioxidant pararneters,SOD , NPSH(which represent GSH) and lipid per oxidation tepresented by thiobarbutric acid reactive subestances (TBARS) were determined and compared to both normal control group and gentamycin-ureamic group.. The results revealed that, valsartan in the lower dose (3mg/kg/day) which caused minimal reduction of arterial blood pressureri showed nephroprotective qffect while the higher dose (12mg/kg/dcry) which caused significant reduction of arterial blood pressure, exage rated gentamycin induced acute renal failure. These results suggest that angiotensin II may be involved in the pathogenesis of gentamycin induced acute renal failure. Also, the nephroprotective effect of ATI blockers in this model is inversly related to the arterial blood pressure lowering action of these drugs