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 |
