The effect of a nitric oxide donor on endogenous endothelin-1 expression in renal ischemia/reperfusion injury

Jeong, Gyu-Young; Chung, Ku Yong; Lee, Woo Jung; Kim, Yu Seun; Sung, Sun Hee

doi:10.1016/j.transproceed.2004.08.119

Cited by 20 publications

(10 citation statements)

References 6 publications

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“…Table 3 summarizes the results of several studies that have reported the effects of NO donors, L-arginine supplementation, and pharmacological and genetic inhibition of NOS in renal I/R injury. The administration of NO donors such as sodium nitroprusside, molsidomine, and FK-409 is beneficial in renal I/R injury (19,24,31,42). L-Arginine supplementation and NOS inhibitors have shown varying results (4,24,37,41,43,50).…”

Section: Discussionmentioning

confidence: 99%

Effects of sodium nitrite on ischemia-reperfusion injury in the rat kidney

Basireddy

Isbell²,

Teng³

et al. 2006

American Journal of Physiology-Renal Physiology

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. Effects of sodium nitrite on ischemia-reperfusion injury in the rat kidney. Am J Physiol Renal Physiol 290: F779 -F786, 2006. First published November 8, 2005 doi:10.1152/ajprenal.00334.2005.-Reactive oxygen and nitrogen species play a key role in the pathophysiology of renal ischemiareperfusion (I/R) injury. Recent studies have shown that nitrite (NO 2 Ϫ ) serves as an endogenous source of nitric oxide (NO), particularly in the presence of hypoxia and acidosis. Nanomolar concentrations of NO 2 Ϫ reduce injury following I/R in the liver and heart in vivo. The purpose of this study was to evaluate the role of NO 2 Ϫ in renal I/R injury. Male Sprague-Dawley rats underwent a unilateral nephrectomy followed by 45 min of ischemia of the contralateral kidney or sham surgery under isoflurane anesthesia. Animals received normal saline, sodium NO 2 Ϫ , or sodium nitrate (NO 3 Ϫ ; 1.2 nmol/g body wt ip) at 22.5 min after induction of ischemia or 15 min before ischemia. A separate set of animals received saline, NO 2 Ϫ , or NO 3 Ϫ (0.12, 1.2, or 12 nmol/g body wt iv) 45 min before ischemia. Serum creatinine and blood urea nitrogen were increased following I/R injury but were not significantly different among treatment groups at 24 and 48 h after acute renal injury. Interestingly, NO 3 Ϫ administration appeared to worsen renal injury. Histological scoring for loss of brush border, tubular necrosis, and red blood cell extravasation showed no significant differences among the treatment groups. The results indicate that, contrary to the protective effects of NO 2 Ϫ in I/R injury of the liver and heart, NO 2 Ϫ does not provide protection in renal I/R injury and suggest a unique metabolism of NO 2 Ϫ in the kidney. nitric oxide; nitrate; acute renal injury; tubular necrosis; hypoxia ACUTE RENAL FAILURE (ARF) remains a major cause of morbidity and mortality in hospitalized patients (45). In addition, renal dysfunction develops in 5% of all general surgical patients and complicates the course of recovery in 15-25% of critically ill patients (34). Current therapeutic options are limited to supportive measures and renal replacement therapy, necessitating the need for the development of more viable therapies for ARF.

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Section: Discussionmentioning

confidence: 99%

Effects of sodium nitrite on ischemia-reperfusion injury in the rat kidney

Basireddy

Isbell²,

Teng³

et al. 2006

American Journal of Physiology-Renal Physiology

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“…Several agents with antioxidant properties have been shown to be renoprotective in animal models of ischemia/reperfusion [33,34] and nephrotoxicity [35], not only decreasing ROS but also restoring the antioxidant enzymes. Enhancing nitric oxide ameliorates ischemia/reperfusion, possibly by suppressing ET-1, a powerful vasoconstrictor acting via ETB receptors [26,36].…”

Section: Ischemia/reperfusion Injury and Acute Renal Failurementioning

confidence: 99%

Oxidative stress and nitric oxide in kidney function

Araújo

Welch

2006

Current Opinion in Nephrology &Amp; Hypertension

100

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Several new approaches and provocative findings have emerged over the last year. A regulatory role for nitric oxide in the control of the renal microcirculation and as a participant in tubule function is further described. New information of the cause and possible prevention of acute and chronic renal failure has also been produced in the last year. These advances demonstrate the value of research in the normal and pathological roles of oxidative stress and nitric oxide in the kidney.

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“…The proinflammatory cytokine interleukin (IL) 6, markers of lipid peroxidation such as 8‐isoprostane, and myeloperoxidase (MPO) activity as a measure of neutrophil infiltration are sensitive means of determining the level of IR injury11. Injury also increases the expression of endothelin (ET) 1, a potent vasoconstrictor that further restricts blood flow12. Severe IR injury has a strong association with DGF and PNF7.…”

Section: Introductionmentioning

confidence: 99%