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1 Renal Research Centre, Unversity of Queensland, Brisbane, Queensland, Australia; Centre for Chronic Disease, Unversity of Queensland, Australia
2 Discipline of Molecular and Cellular Pathology, Unversity of Queensland, Brisbane, Queensland, Australia
3 Renal Research Centre, Unversity of Queensland, Brisbane, Queensland, Australia
4 Renal Research Centre, Unversity of Queensland, Brisbane, Queensland, Australia; Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, New Zealand
* To whom correspondence should be addressed. E-mail: zoltan.endre{at}chmeds.ac.nz.
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 NO derived from iNOS. We investigated renal endothelial dysfunction in kidneys from Sprague-Dawley rats by assessing autoregulation and endothelium-dependent vasorelaxation 24 hours after unilateral (U) or bilateral (B) renal artery occlusion for 30 or 60 minutes and in sham-operated controls. Although renal failure was induced in all degrees of ischemia, neither endothelial dysfunction nor altered facilitation of autoregulation by 75pM 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 preserved in B60 kidneys. Increasing angiotensin II concentration restored autoregulation and increased RVR in B60 kidneys; this facilitated autoregulation and increase in RVR was abolished by 100µM furosemide. Autoregulation was enhanced by L-NAME. Peri-ischemic inhibition of iNOS 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 tubuloglomerular feedback (TGF) 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 loss of GFR. Arteriolar endothelial dysfunction after prolonged IARF is predominantly functional rather than structural.
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