HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/6/H3542    most recent 00977.2007v1 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 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.

Heme oxygenase-1 induction improves ischemic renal failure: role of nitric oxide and peroxynitrite

¹Departamento de Fisiología, Facultad de Medicina, Universidad de Murcia and ²Servicio de Análisis Clínicos, Unidad de Investigación, ³Servicio de Cirugía, and ⁴Servicio de Nefrología, Hospital Universitario "Virgen de la Arrixaca," Murcia, Spain

Submitted 23 August 2007 ; accepted in final form 19 September 2007

The present study evaluated the effects of heme oxygenase-1 (HO-1) induction on the changes in renal outer medullary nitric oxide (NO) and peroxynitrite levels during 45-min renal ischemia and 30-min reperfusion in anesthetized rats. Glomerular filtration rate (GFR), outer medullary blood flow (OMBF), HO and nitric oxide synthase (NOS) isoform expression, and renal low-molecular-weight thiols (–SH) were also determined. During ischemia significant increases in NO levels and peroxynitrite signal were observed (from 832.1 ± 129.3 to 2,928.6 ± 502.0 nM and from 3.8 ± 0.7 to 9.0 ± 1.6 nA before and during ischemia, respectively) that dropped to preischemic levels during reperfusion. OMBF and –SH significantly decreased after 30 min of reperfusion. Twenty-four hours later, an acute renal failure was observed (GFR 923.0 ± 66.0 and 253.6 ± 55.3 µl·min^–1·g kidney wt^–1 in sham-operated and ischemic kidneys, respectively; P < 0.05). The induction of HO-1 (CoCl₂ 60 mg/kg sc, 24 h before ischemia) decreased basal NO concentration (99.7 ± 41.0 nM), although endothelial and neuronal NOS expression were slightly increased. CoCl₂ administration also blunted the ischemic increase in NO and peroxynitrite (maximum values of 1,315.6 ± 445.6 nM and 6.3 ± 0.5 nA, respectively; P < 0.05), preserving postischemic OMBF and GFR (686.4 ± 45.2 µl·min^–1·g kidney wt^–1). These beneficial effects of CoCl₂ on ischemic acute renal failure seem to be due to HO-1 induction, because they were abolished by stannous mesoporphyrin, a HO inhibitor. In conclusion, HO-1 induction has a protective effect on ischemic renal failure that seems to be partially mediated by decreasing the excessive production of NO with the subsequent reduction in peroxynitrite formation observed during ischemia.

cobalt chloride; nitric oxide stores; Western blot; nitric oxide synthase; peroxynitrite amperometry; nitric oxide voltammetry

This article has been cited by other articles:

				J. Bylander, Q. Li, G. Ramesh, B. Zhang, W. B. Reeves, and J. S. Bond Targeted disruption of the meprin metalloproteinase {beta} gene protects against renal ischemia-reperfusion injury in mice Am J Physiol Renal Physiol, March 1, 2008; 294(3): F480 - F490. [Abstract] [Full Text] [PDF]