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Am J Physiol Renal Physiol 291: F619-F628, 2006. First published March 28, 2006; doi:10.1152/ajprenal.00302.2005
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Renal endothelial dysfunction and impaired autoregulation after ischemia-reperfusion injury result from excess nitric oxide

Zhengrong Guan,1,2 Glenda Gobé,3 Desley Willgoss,1 and Zoltán H. Endre1,4

1Renal Research Centre and 2Centre for Chronic Disease, Discipline of Medicine, and 3Discipline of Molecular and Cellular Pathology, University of Queensland, Queensland, Australia; and 4Department of Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand

Submitted 27 July 2005 ; accepted in final form 2 March 2006

Endothelial dysfunction in ischemic acute renal failure (IARF) has been attributed to both direct endothelial injury and to altered endothelial nitric oxide synthase (eNOS) activity, with either maximal upregulation of eNOS or inhibition of eNOS by excess nitric oxide (NO) derived from iNOS. We investigated renal endothelial dysfunction in kidneys from Sprague-Dawley rats by assessing autoregulation and endothelium-dependent vasorelaxation 24 h after unilateral (U) or bilateral (B) renal artery occlusion for 30 (U30, B30) or 60 min (U60, B60) and in sham-operated controls. Although renal failure was induced in all degrees of ischemia, neither endothelial dysfunction nor altered facilitation of autoregulation by 75 pM angiotensin II was detected in U30, U60, or B30 kidneys. Baseline and angiotensin II-facilitated autoregulation were impaired, methacholine EC50 was increased, and endothelium-derived hyperpolarizing factor (EDHF) activity was preserved in B60 kidneys. Increasing angiotensin II concentration restored autoregulation and increased renal vascular resistance (RVR) in B60 kidneys; this facilitated autoregulation, and the increase in RVR was abolished by 100 µM furosemide. Autoregulation was enhanced by N{omega}-nitro-L-arginine methyl ester. Peri-ischemic inhibition of inducible NOS ameliorated renal failure but did not prevent endothelial dysfunction or impaired autoregulation. There was no significant structural injury to the afferent arterioles with ischemia. These results suggest that tubuloglomerular feedback is preserved in IARF but that excess NO and probably EDHF produce endothelial dysfunction and antagonize autoregulation. The threshold for injury-producing, detectable endothelial dysfunction was higher than for the loss of glomerular filtration rate. Arteriolar endothelial dysfunction after prolonged IARF is predominantly functional rather than structural.

isolated perfused rat kidney; tubuloglomerular feedback; angiotensin II-facilitated autoregulation; endothelium-derived hyperpolarizing factor


Address for reprint requests and other correspondence: Z. H. Endre, Dept. of Medicine, Christchurch School of Medicine and Health Sciences, Univ. of Otago, PO Box 4345, Christchurch, New Zealand (e-mail: rowena.fisher{at}chmeds.ac.nz)




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