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This Article Full Text Full Text (PDF) All Versions of this Article: 292/4/R1494    most recent 00540.2006v1 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 (1) Citing Articles via Google Scholar Google Scholar Articles by Piotrkowski, B. Articles by de Cavanagh, E. M. V. Search for Related Content PubMed PubMed Citation Articles by Piotrkowski, B. Articles by de Cavanagh, E. M. V.

RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Mitochondrial function and nitric oxide metabolism are modified by enalapril treatment in rat kidney

¹Physical Chemistry-PRALIB, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina; and ²Department of Nutrition, University of California, Davis, California

Submitted 27 July 2006 ; accepted in final form 11 December 2006

The renal and cardiac benefits of renin-angiotensin system (RAS) inhibition in hypertension exceed those attributable to blood pressure reduction, and seem to involve mitochondrial function changes. To investigate whether mitochondrial changes associated with RAS inhibition are related to changes in nitric oxide (NO) metabolism, four groups of male Wistar rats were treated during 2 wk with a RAS inhibitor, enalapril (10 mg·kg^–1·day^–1; Enal), or a NO synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME) (1 mg·kg^–1·day^–1), or both (Enal+L-NAME), or were untreated (control). Blood pressure and body weight were lower in Enal than in control. Electron transfer through complexes I to III and cytochrome oxidase activity were significantly lower, and uncoupling protein-2 content was significantly higher in kidney mitochondria isolated from Enal than in those from control. All of these changes were prevented by L-NAME cotreatment and were accompanied by a higher production/bioavailability of kidney NO. L-NAME abolished mitochondrial NOS activity but failed to inhibit extra-mitochondrial kidney NOS, underscoring the relevance of mitochondrial NO in those effects of enalapril that were suppressed by L-NAME cotreatment. In Enal, kidney mitochondria H₂O₂ production rate and MnSOD activity were significantly lower than in control, and these effects were not prevented by L-NAME cotreatment. These findings may clarify the role of NO in the interactions between RAS and mitochondrial metabolism and can help to unravel the mechanisms involved in renal protection by RAS inhibitors.

angiotensin; membrane potential; uncoupling protein; N-nitro-L-arginine methyl ester; reactive oxygen species

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