THE RENIN-ANGIOTENSIN SYSTEM IN AMINOGLYCOSIDE-INDUCED ACUTE-RENAL-FAILURE

  • 1 January 1982
    • journal article
    • research article
    • Vol. 220  (2) , 433-439
Abstract
To examine the role of the renin-angiotensin [A] system in aminoglycoside-induced acute renal failure, rats were given gentamicin (80 mg/kg per day), gentamicin + captopril (an A-converting enzyme inhibitor), captopril alone or saline sham injections, for 10 days. Blood pressure, Na excretion, urine osmolality and creatinine clearance were measured 4 times during treatment. Plasma renin activity, A I-converting enzyme and renal histology were determined at sacrifice. Although A I-convering enzyme activity was suppressed by captopril treatment, the addition of captopril failed to consistently influence blood pressure or urine osmolality. It did not promote natriuresis in the face of gentamicin toxicity. Creatinine clearance decreased progressively in groups receiving gentamicin and was lowest (P < 0.05) in the groups receiving gentamicin + captopril. Captopril did not prevent the development of tubular epithelial nor glomerular endothelial changes associated with gentamicin toxicity. Rats received captopril for 3 days prior, before receiving the gentamicin + captopril regimen for 10 days. Captopril pretreatment did not influence the results. A pivotal role for the renin-A system in the production of the decreased glomerular filtration rate observed in nephrotoxic acute renal failure induced by gentamicin in rats is not supported.