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This Article Full Text Full Text (PDF) All Versions of this Article: 289/5/R1459    most recent 00746.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Salom, M. G. Articles by Fenoy, F. J. Search for Related Content PubMed PubMed Citation Articles by Salom, M. G. Articles by Fenoy, F. J.

RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Renal ischemia induces an increase in nitric oxide levels from tissue stores

¹Departamento de Fisiología, Facultad de Medicina, and ²Servicio de apoyo a las ciencias experimentales, Universidad de Murcia, Murcia, Spain; and ³Departamento de Fisiología, Universidad de La Laguna, Tenerife, Spain

Submitted 3 November 2004 ; accepted in final form 31 May 2005

Tissue nitric oxide (NO) levels increase dramatically during ischemia, an effect that has been shown to be partially independent from NO synthases. Because NO is stored in tissues as S-nitrosothiols and because these compounds could release NO during ischemia, we evaluated the effects of buthionine sulfoximine (BSO; an intracellular glutathione depletor), light stimulation (which releases NO, decomposing S-nitrosothiols), and N-acetyl-L-cysteine (a sulfhydryl group donor that repletes S-nitrosothiols stores) on the changes in outer medullary NO concentration produced during 45 min of renal artery occlusion in anesthetized rats. Renal ischemia increased renal tissue NO concentration (+223%), and this effect was maintained along 45 min of renal arterial blockade. After reperfusion, NO concentration fell below preischemic values and remained stable for the remainder of the experiment. Pretreatment with 10 mg/kg nitro-L-arginine methyl ester (L-NAME) decreased significantly basal NO concentration before ischemia, but it did not modify the rise in NO levels observed during ischemia. In rats pretreated with 4 mmol/kg BSO and L-NAME, ischemia was followed by a transient increase in renal NO concentration that fell to preischemic values 20 min before reperfusion. A similar response was observed when the kidney was illuminated 40 min before the ischemia. The coadministration of 10 mg/kg iv N-acetyl-L-cysteine with BSO + L-NAME restored the increase in NO levels observed during renal ischemia and prevented the depletion of renal thiol groups. These results demonstrate that the increase in renal NO concentration observed during ischemia originates from thiol-dependent tissue stores.

voltammetry; nitrosothiols; N-acetyl-L-cysteine; buthionine sulfoximine; photosensitive nitric oxide release

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