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Acta bioquímica clínica latinoamericana

versión On-line ISSN 1851-6114

Resumen

DE LA CRUZ RODRIGUEZ, Lilia Cristina; POSLEMAN, Sara Emilia; ARAUJO, Carmen Rosa  y  REY, María Rosario. The nitric oxide in experimental nephrotoxicity induced by ciclosporine A. Acta bioquím. clín. latinoam. [online]. 2005, vol.39, n.1, pp. 5-10. ISSN 1851-6114.

The acute nephrotoxicity induced by cyclosporine A (CyA) is characterized by a renal plasmatic flux decrease. The nitric oxide (NO), which is a vasodilating factor, seems to be the explanation for nephrotoxicity by CyA. The aim of this work is to evaluate the effect of NO induced by L- Arginine (L- Arg) in experimental nephrotoxicity by CyA. The studied population consisted on male rats divided into 4 groups (n = 8): A, B,C and D. Groups A and B were treated with standard diet, and groups C and D were suplemented by 500 mg/kg of food of L-Arg. Groups B and D were treated with 0,1 ml of 50 mg/ml of CyA solution during 7 days. The glomerular filtration was evaluated through serum creatinine and creatinine clearance. The serum creatinine of group D, treated with L-Arg and CyA, was significantly greater than in the other groups (p < 0.05). The creatinine clearance decreased in groups B and D (treated with CyA). NO was investigated by the excretion of urinary metabolites : nitrite + nitrate in 24 h urinary samples. The oxide nitric values were significantly greater in groups C and D, treated with L-Arg (p < 0.05), but there were no significant differences of B in relation to A. Anatomo-histological changes were evaluated. There was an increase kidney's size. Hipotrophic renal parenchima and renal-tubule dilatation with cellular descamation were observed with histological methods. Therefore: If CyA has a vasoconstrictor effect on the afferent arteriole together with a decrease in the medular and cortical perfusion, the increase in the production of NO provokes vasodilatation and induces to a severe renal injure which makes itself more powerful in the presence of CyA that would increase the production of Nitric Oxide Sintetase (NOS) via iNOS mRNA.

Palabras clave : Nephrotoxicity; Cyclosporine A; Nitric oxide.

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