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Am J Physiol Renal Physiol 274: F791-F798, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 4, F791-F798, April 1998

Role of NO in cyclosporin nephrotoxicity: effects of chronic NO inhibition and NO synthases gene expression

Norma A. Bobadilla1, Gerardo Gamba2, Edilia Tapia1, Romeo García-Torres3, Alexis Bolio1, Pedro López-Zetina1, and Jaime Herrera-Acosta1

Departments of 1 Nephrology and 3 Pathology, Instituto Nacional de Cardiología Ignacio Chávez; and 2 Molecular Physiology Unit, Department of Nephrology and Mineral Metabolism,Instituto Nacional de la Nutrición Salvador Zubirán and Instituto de Investigaciones Biomédicas, National University of Mexico, Mexico City CP 14080, Mexico

The role of nitric oxide (NO) during cyclosporin renal vasoconstriction was evaluated by glomerular hemodynamic and histological changes produced by chronic NO synthesis inhibition and neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) NO synthases mRNA expression in renal cortex and medulla. Uninephrectomized rats treated during 7 days with vehicle (Veh), cyclosporin A (CsA) 30 mg/kg, CsA + nitro-L-arginine methyl ester (L-NAME), and Veh + L-NAME (10 mg/dl) in the drinking water were studied. Increase in arterial pressure and afferent and efferent resistances, as well as decrease in glomerular plasma flow, ultrafiltration coefficient, and single-nephron glomerular filtration rate were significantly greater with CsA + L-NAME than with CsA alone. The increase in afferent resistance was higher with CsA + L-NAME than with Veh + L-NAME. In addition, glomerular thrombosis, proximal tubular vacuolization, and arteriolar thickening were more prominent. In renal cortex, eNOS mRNA expression exhibited a 2.7-fold increase in CsA, whereas, in medulla, nNOS and iNOS expression were lower in CsA than in Veh, while eNOS tended to increase. Our results support the hypothesis that NO synthesis is enhanced at cortical level during CsA nephrotoxicity, counterbalancing predominantly preglomerular vasoconstriction. Higher NO production could be the result of increased eNOS mRNA expression.

micropuncture studies; preglomerular vasoconstriction; renal histopathology; reverse transcription-polymerase chain reaction; nitric oxide


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