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1 Departamento de Fisiologia, Universidad de Murcia, Murcia, Spain
2 Servicio de Apoyo a las Ciencias Experimentales, Universidad de Murcia, Murcia, Spain
3 Departamento de Fisiologia, Universidad de La Laguna, La Laguna, Tenerife, Spain
* To whom correspondence should be addressed. E-mail: mgsalom{at}um.es.
Tissular 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 these compounds could release NO during ischemia, in the present study 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 sulphydryl 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 tissular NO concentration (+223%), and this effect was maintained along 45 minutes of renal arterial blockade. After reperfusion, NO concentration fell below preischemic values and remained stable for the remainder of the experiment. Pre-treatment with L-NAME (10 mg/kg) decreased significantly basal NO concentration before ischemia but it did not modify the rise in NO levels observed during ischemia. In rats pre-treated with BSO (4 mmol/kg) and L-NAME, ischemia was followed by a transient increase in renal NO concentration that fell to preischemic values 20 minutes before reperfusion. A similar response was observed when the kidney was illuminated 40 min before the ischemia. The co administration of N-acetyl-L-cysteine (10 mg/kg, iv) with BSO+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 tissular stores.
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