Atrial natriuretic peptide protects against acute ischemic renal failure in the rat.

Shaw, Sidney; Weidmann, P; Hodler, J; Zimmermann, Arthur; Paternostro, A.

doi:10.1172/jci113197

Cited by 135 publications

(64 citation statements)

References 18 publications

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“…ANP also induces redistribution of renal medullary blood flow (Davis and Briggs 1987). Furthermore, ANP has been shown to improve renal function in rats with ischemic acute renal failure by improving renal adenosine triphosphate regeneration after reperfusion (Nakamoto et al 1987), thereby preserving the glomerular filtration rate and thus reducing renal tissue damage (Shaw et al 1987). However, the mechanisms of the renoprotective effects of ANP remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Chujo

Ueki

Asaga

et al. 2008

Tohoku J. Exp. Med.

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Activated neutrophils have been implicated in the development of ischemia/reperfusion (I/R)-induced renal failure. Cytokine-induced neutrophil chemoattractant-1 (CINC-1), a major factor in acute inflammation, is responsible for the activation of neutrophils and for neutrophil chemotaxis to sites of injury. Atrial natriuretic peptide (ANP), a hormone synthesized by the cardiac atria, was shown to possess anti-inflammatory potential due to its potency to inhibit the production of inflammatory mediators. We examined whether the human form of ANP attenuates I/R-induced renal injury by reducing neutrophil activation in a rat model. Male Wistar rats weighing 200-240 g were observed for 24 h after reperfusion following 45-min renal ischemia. Rats were intravenously administered alphahuman ANP (α -hANP, 0.2 μ g/kg/min) beginning immediately after ischemia and continuing for 2 h after reperfusion. CINC-1 and myeloperoxidase (MPO) concentrations were measured to assess activation of the infiltrating neutrophil. Blood urea nitrogen and serum creatinine and urinary N-acetyl β -d-glucosaminidase (NAG) were measured as indicators of glomerular function and as a specific indicator of proximal tubular function, respectively. α -hANP significantly inhibited I/R-induced increases in renal CINC-1 and MPO concentrations. α -hANP also reduced I/R-induced increases in the concentrations of blood urea nitrogen and serum creatinine, and improved histopathologic changes, including acute tubular necrosis. These findings indicate that α -hANP attenuates I/R-induced acute renal injury, at least in part by reducing neutrophil activation, and may be useful in surgeries, associated with renal ischemia, as well as in renal transplantation.human atrial natriuretic peptide; neutrophils; kidney; ischemia/reperfusion; cytokine-induced neutrophil chemoattractant-1. Tohoku

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Section: Discussionmentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Chujo

Ueki

Asaga

et al. 2008

Tohoku J. Exp. Med.

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“…It is likely that cyclic GMP, a second messenger induced by NO, is elaborated by the kidney during IL-2 therapy (68,73,74). It has been shown that atrial natriuretic factor, a peptide with vasodilating and diuretic/natriuretic properties, ameliorates, via cyclic GMP, the severity of acute renal failure (75,76).…”

Section: Discussionmentioning

confidence: 99%

Evidence for cytokine-inducible nitric oxide synthesis from L-arginine in patients receiving interleukin-2 therapy.

Hibbs¹,

Westenfelder²,

Taintor³

et al. 1992

J. Clin. Invest.

481

160

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An interferon-'y, tumor necrosis factor, and interleukin-1-inducible, high-output pathway synthesizing nitric oxide (NO) from L-arginine was recently identified in rodents. High-dose interleukin-2 (IL-2) therapy is known to induce the same cytokines in patients with advanced cancer. Therefore, we examined renal cell carcinoma (RCC; n = 5) and malignant melanoma (MM; n = 7) patients for evidence of cytokine-inducible NO synthesis. Activity of this pathway was evaluated by measuring serum and urine nitrate (the stable degradation product of NO) during IL-2 therapy. IL-2 administration caused a striking increase in NO generation as reflected by serum nitrate levels (10-and 8-fold increase IP < 0.001, P < 0.0031 for RCC and MM patients, respectively) and 24-h urinary nitrate excretion (6.5-and 9-fold increase [both P < 0.0011 for RCC and MM patients, respectively). IL-2-induced renal dysfunction made only a minor contribution to increased serum nitrate levels. Metabolic tracer studies using L-[guanidino-5N2Jarginine demonstrated that the increased nitrate production was derived from a terminal guanidino nitrogen atom of L-arginine. Our results showing increased endogenous nitrate synthesis in patients receiving IL-2 demonstrate for the first time that a cytokine-inducible, highoutput L-arginine/NO pathway exists in humans. (J. Clin. Invest. 1992. 89:867-877.) Key words: acute renal failure * malignant melanoma * nitrate * nitrite * renal cell carcinoma

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“…The reno-protective effect of ANP during endotoxemia could therefore be traced in the absence of renal nerves, although the improvement in the GFR value was relatively minor, considering the massive pharmacological dose of ANP employed. Recent studies show a therapeutic potential of the ANP for preserving renal function after renal ischemia [8,9]. ANP administration immediately after the ischemic insult significantly improves renal structure and function as assessed by GFR and ATP generation [9,10], the effects of which are not seen with other vasodilators such as acetylcholine [27] and nitroprusside [28].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies show a therapeutic potential of the ANP for preserving renal function after renal ischemia [8,9]. ANP administration immediately after the ischemic insult significantly improves renal structure and function as assessed by GFR and ATP generation [9,10], the effects of which are not seen with other vasodilators such as acetylcholine [27] and nitroprusside [28]. The renal effect of ANP in the renal ischemic injury may be due to an increase in intraglomerular pressure which resulted from a unique combination of preglomerular arteriolar dilatation and efferent constriction [29].…”

Section: Discussionmentioning

confidence: 99%

“…Most often, where Et is associated with acute renal failure, it appears to be largely acute tubular necrosis [6,7]. Recent studies have reported beneficial effects of atrial natriuretic peptide (ANP) in limiting ischemic renal injury [8,9]. In animal models of acute ischemic renal damage, ANP decreases renal vascular resistance [8,10], increases renal blood flow [11,12] and consequently, increases GFR [13,14], which suggests a possible hemodynamic action of ANP in recovery from renal injury induced by an Et.…”

Section: Gram-negativementioning

confidence: 99%

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Atrial Natriuretic Peptide Has No Potential to Protect Against Endotoxin-lnduced Acute Renal Failure in the Absence of Renal Nerves.

Hiki¹,

Mimura²

1998

Endocr J

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Abstract. Atrial natriuretic peptide (ANP) has been shown to have the potential to restore renal function after ischemic injury, an underlying component of endotoxin (Et)-induced acute renal failure, and is known to counteract renal sympathetic nerve activity in renal function. We have recently found that renal denervation restores the Et-induced renal dysfunction. The purpose of this study was to examine effects of ANP infusion on the Et-induced acute renal failure in the absence of renal nerves. Ten to 14 days after bilateral renal denervation (DNX), Wistar rats (250 to 300 g body wt) were used in the acute experiment.Rats with intact renal nerves (INN) served as controls. Following control clearance measurements, rats were intravenously injected with 4 mg/kg Et (Escherichia coli, 055: B5). During endotoxemia, rats were infused with 10 µg/kg/h ANP or saline vehicle. Et injection reduced the glomerular filtration rate (GFR) significantly in saline-infused INN and DNX rats. ANP infusion restored the greatly reduced GFR to the pre-endotoxemia level in DNX rats but not in INN rats. There was significant difference between the ANP-and saline-infused DNX rats in the percentage change relative to the basal GFR value during the ANP infusion period. ANP infusion did not improve the hyponatriuresis and oliguria after Et administration, which is independent of renal nerves. In conclusion, ANP infusion has a minor reno-protective effect in rats with Et-induced acute renal failure in the absence of the renal nerves.

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Atrial natriuretic peptide protects against acute ischemic renal failure in the rat.

Cited by 135 publications

References 18 publications

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Evidence for cytokine-inducible nitric oxide synthesis from L-arginine in patients receiving interleukin-2 therapy.

Atrial Natriuretic Peptide Has No Potential to Protect Against Endotoxin-lnduced Acute Renal Failure in the Absence of Renal Nerves.

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