Dopamine protects gentamicin early induced nephrotoxicity in Sprague–Dawley rats

Routine therapeutic use of dopamine has been shown to influence renal hemodynamic response through removing contractile effects of nephrotoxicants on mesangial cells and subsequent interaction with locally expressed prostaglandin subtypes (PGE2 and PGI2). To determine the way in which the amino acid managed to preserve Sprague–Dawley rats against gentamicin-induced nephrotoxicity, a randomized prospective study was carried out. In this study, 40 healthy rats were randomly assigned in four trials to receive either normal saline, gentamicin, gentamicin plus dopamine, or dopamine for 9 days. Administration of gentamicin at a dose of 80 mg kg⁻¹ day⁻¹ reduced the creatinine clearance as result of early hemodynamic toxicity, and tubular reabsorption of electrolytes after phospholipiduria and urinary activity of tubular enzymes. H&E histopathology revealed acute tubular necrosis with cast formation triggered by gentamicin over 9 days of experiment, in addition to interstitial nephritis and tubular epithelial loss. Further biochemical studies showed protecting effects of supplemented dopamine, including slow down in the urinary enzyme activity, modest to moderate phospholipiduria with recovery in the renal clearance and the ATPase activity up to 50% when compared to saline- and gentamicin-treated rats. Normal glomerular and tubular function on recovery from toxic renal failure led us to conclude that renovascular effects of dopamine were early attributed to glomerular preservation, whereas the tubule function prepared by the amino acid was just a consequent.