Relative roles of endothelin-1 and angiotensin II in experimental post-ischaemic acute renal failure

Jerkić, Mirjana; Miloradović, Zoran; D, Jovović; Mihailović-Stanojević, Nevena; Elena, Juan Vicente Rivas; Nastić-Mirić, D; Grujić-Adanja, G; Rodríguez-Barbero, Alicia; Marković-Lipkovski, Jasmina; Vojvodić, Srećko B; Manero, Marta Vicens; Prieto, Marta Pérez; López‐Novoa, José M.

doi:10.1093/ndt/gfg521

Cited by 44 publications

(45 citation statements)

References 15 publications

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“…After clamp removal, the abdominal incision was closed by several sutures, and the rats were allowed to fully wake up and to recover and were placed in metabolic cages. The cages had been cleaned with germicidal soap to prevent nitrate and/or nitrite formation by bacteria [34]. A 24-hour reperfusion period was allowed for urine collection, with free access to water and chow.…”

Section: Methodsmentioning

confidence: 99%

Allopurinol and Enalapril Failed to Conserve Urinary NOx and Sodium in Ischemic Acute Renal Failure in Spontaneously Hypertensive Rats

Radović

Miloradović²,

Popović³

et al. 2006

Am J Nephrol

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Background: Ischemia-reperfusion-induced acute renal failure (ARF) is associated with a high mortality in patients with hypertension and with an unfavorable outcome of kidney transplants from marginal donors. Aim: The influence of allopurinol and enalapril on urinary nitrate/nitrite (UNOx), glomerular filtration rate, plasma and urinary sodium, and hemodynamic parameters was examined in spontaneously hypertensive rats (SHR) with ARF. Methods: ARF was induced by right-kidney removal and clamping the left renal artery for 40 min in 50 male 26-week-old SHR weighing 300 ± 23 g. The rats were randomly allocated to five groups: (1) sham operated; (2) ARF; (3) ARF after pretreatment with 40 mg/kg allopurinol; (4) ARF after pretreatment with 40 mg/kg enalapril, and (5) ARF after pretreatment with 40 mg/kg allopurinol and 40 mg/kg enalapril. Creatinine clearance, UNOx (Griess reaction), cardiac output (dye dilution technique), mean arterial blood pressure, and renal blood flow were measured 24 h after reperfusion. Total vascular resistance and renal vascular resistance were calculated and compared between the groups. Results: A nonsignificant decrease was found in both daily UNOx excretion and creatinine clearance when pretreated ARF groups and the ARF group without pretreatment were compared (p > 0.05). Significantly lower plasma sodium values (139.5 ± 4.86 mmol/l) in the allopurinol-pretreated ARF group were found than in the ARF group without pretreatment, in the ARF group pretreated with enalapril, and in the sham SHR group (p = 0.029). The urinary sodium loss was greater in the enalapril-pretreated than in the allopurinol-pretreated ARF group (p = 0.047). Allopurinol and/or enalapril pretreatment decreased total vascular resistance (p = 0.003) in comparison with the sham SHR group. Conclusion: Neither allopurinol nor enalapril nor both were protective against ischemia-reperfusion injury in SHR, nor altered glomerular filtration rate and UNOx in a favorable direction.

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Section: Methodsmentioning

confidence: 99%

Allopurinol and Enalapril Failed to Conserve Urinary NOx and Sodium in Ischemic Acute Renal Failure in Spontaneously Hypertensive Rats

Radović

Miloradović²,

Popović³

et al. 2006

Am J Nephrol

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“…This results in a local imbalance of vasoactive substances, with enhanced release of vasoconstrictors such as endothelin and decreased abundance of vasodilators such as endothelium-derived nitric oxide (NO) (2). Endothelin receptor antagonists ameliorate ischemic AKI in animals (18), but human data are lacking. Similarly, both carbon monoxide and carbon monoxide-releasing compounds are protective in animal models of ischemic AKI (19,20), likely through vasodilation and preservation of medullary blood flow, but have not been tested in humans.…”

Section: Alterations In Morphologymentioning

confidence: 99%

Update on Mechanisms of Ischemic Acute Kidney Injury

Devarajan

2006

Journal of the American Society of Nephrology

898

759

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“…These abnormalities in vascular reactivity have been associated with increases in cytosolic Ca 2+ (79); such increases in intracellular Ca 2+ may also cause cell death by inducing the activation of proteases, phospholipases, and pro-apoptotic pathways (80). Of all the vasoconstrictive agents, endothelin seems to be particularly important, because endothelin-1 levels have been found to increase after ischemia, and blockage of the endothelin pathway by endothelin A receptor antagonists (70,76) has been shown to protect against I/R injury. NO can counteract the effects of endothelin after I/R (81).…”

Section: Microvascular Dysfunction and The Balance Between Vasoconstrmentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

238

169

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Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

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Relative roles of endothelin-1 and angiotensin II in experimental post-ischaemic acute renal failure

Abstract: These results suggest that ET-1 blockade is more efficient in improving the early course of post-ischaemic renal injury than ANG II inhibition, and that blockade of ET-1 might be effective in prophylaxis of ischaemic ARF.

Cited by 44 publications

References 15 publications

Allopurinol and Enalapril Failed to Conserve Urinary NOx and Sodium in Ischemic Acute Renal Failure in Spontaneously Hypertensive Rats

Allopurinol and Enalapril Failed to Conserve Urinary NOx and Sodium in Ischemic Acute Renal Failure in Spontaneously Hypertensive Rats

Update on Mechanisms of Ischemic Acute Kidney Injury

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

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