SciELO - Scientific Electronic Library Online

vol.39 número1Marcadores bioquímicos óseos durante la premenopausia en mujeres con baja ingesta habitual de calcio índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados



  • No hay articulos citadosCitado por SciELO

Links relacionados


Acta bioquímica clínica latinoamericana

versión On-line ISSN 1851-6114


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.

        · resumen en Español     · texto en Español     · Español ( pdf )


Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License