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Valdivielso JM, Rivas-Cabañero L, Pérez-Barriocanal F, et al. Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity. Environ Toxicol Pharmacol. 1997;3(2):123-8doi: 10.1016/s1382-6689(97)00148-8.
Valdivielso, J. M., Rivas-Cabañero, L., Pérez-Barriocanal, F., & López-Novoa, J. M. (1997). Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity. Environmental toxicology and pharmacology, 3(2), 123-8. https://doi.org/10.1016/s1382-6689(97)00148-8
Valdivielso, J M, et al. "Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity." Environmental toxicology and pharmacology vol. 3,2 (1997): 123-8. doi: https://doi.org/10.1016/s1382-6689(97)00148-8
Valdivielso JM, Rivas-Cabañero L, Pérez-Barriocanal F, López-Novoa JM. Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity. Environ Toxicol Pharmacol. 1997 Jun 06;3(2):123-8. doi: 10.1016/s1382-6689(97)00148-8. PMID: 21781769.
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Environ Toxicol Pharmacol. 1997 Jun 06;3(2):123-8. doi: 10.1016/s1382-6689(97)00148-8.

Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity.

Environmental toxicology and pharmacology

J M Valdivielso, L Rivas-Cabañero, F Pérez-Barriocanal, J M López-Novoa

Affiliations

  1. Instituto Reina Sof??a de Investigación Nefrológica, Departamento de Fisiolog??a y Farmacolog??a, Facultad de Medicina, Universidad de Salamanca, Avenida Campo Charro s/n, 37?007 Salamanca, Spain.

PMID: 21781769 DOI: 10.1016/s1382-6689(97)00148-8

Abstract

We evaluated the effect of acute or chronic nitric oxide (NO) synthesis activation or inhibition in rats with gentamicin-induced acute renal failure. Rats received gentamicin 100 mg/kg per day for 6 days, or isotonic saline. Some animals of each group also received N(G)-monomethyl-l-arginine (l-NAME, 4 mg/kg per day) or l-arginine (1%) in the drinking water for 6 days (chronic NO synthesis modification). In another experimental set, animals were treated with gentamicin or saline for 6 days and glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured before and after the infusion of l-NAME (50 mg/h per kg) or l-arginine (60 mg/h per kg) (acute NO synthesis modification). Acute l-NAME administration induced a decrease in GFR and RPF both in control and gentamicin treated animals. Chronic l-NAME treatment induced an impairment in GFR only in gentamicin-treated animals. Acute l-arginine administration did not modify renal function in any experimental group whereas chronic l-arginine administration improved renal function only in gentamicin-treated animals. Urinary excretion of N-acetyl-β-d-glucosaminidase and alkaline phosphatase was increased by chronic treatment with l-NAME in both groups, whereas l-arginine had no effect. In conclusion, NO synthesis inhibition aggravates gentamicin-induced renal damage. However, chronic NO synthesis stimulation partially prevents against gentamicin nephrotoxicity, thus suggesting that increased renal NO synthesis during gentamicin-induced nephrotoxicity plays a protector role on renal function.

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