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Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure

BACKGROUND: The pathomechanism of acute hepatorenal syndrome (HRS), a particular form of acute renal failure that occurs in the course of acute liver injury, is still poorly understood. The aim of our study was to estimate the influence of the activation and inhibition of the nitric oxide pathway on...

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Autores principales: Saracyn, Marek, Ząbkowski, Tomasz, Zdanowski, Robert, Brytan, Marek, Patera, Janusz, Nowak, Zbigniew, Kade, Grzegorz, Wańkowicz, Zofia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186324/
https://www.ncbi.nlm.nih.gov/pubmed/25270512
http://dx.doi.org/10.12659/MSM.890757
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author Saracyn, Marek
Ząbkowski, Tomasz
Zdanowski, Robert
Brytan, Marek
Patera, Janusz
Nowak, Zbigniew
Kade, Grzegorz
Wańkowicz, Zofia
author_facet Saracyn, Marek
Ząbkowski, Tomasz
Zdanowski, Robert
Brytan, Marek
Patera, Janusz
Nowak, Zbigniew
Kade, Grzegorz
Wańkowicz, Zofia
author_sort Saracyn, Marek
collection PubMed
description BACKGROUND: The pathomechanism of acute hepatorenal syndrome (HRS), a particular form of acute renal failure that occurs in the course of acute liver injury, is still poorly understood. The aim of our study was to estimate the influence of the activation and inhibition of the nitric oxide pathway on the water/sodium balance and development of acute renal failure in the course of HRS. MATERIAL/METHODS: We used male Sprague-Dawley rats in the acute galactosamine (Ga1N) model of HRS. The nitric oxide synthase (NOS) inhibitors L-NAME and L-arginine were administered intraperitoneally before and after liver damage. RESULTS: HRS developed in all tested groups. L-NAME increased osmotic clearance and urine volume more effectively before liver injury. Furthermore, administration of L-NAME increased creatinine clearance both before and after Ga1N injection. A double dose of L-NAME did not yield further improvement before Ga1N injection, but improved creatinine clearance after Ga1N intoxication. Injection of L-arginine increased sodium excretion and urine volume, but only after liver injury. Moreover, L-arginine injected after Ga1N caused significant improvement of the creatinine clearance in a dose-dependent manner. CONCLUSIONS: Our study shows that inhibition of the nitric oxide pathway improves parameters of water and sodium balance and prevents development of acute renal failure in the course of acute liver injury and liver failure. Activation of the nitric oxide system also has a favorable influence on water/sodium balance and renal failure, but only after liver injury.
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spelling pubmed-41863242014-10-06 Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure Saracyn, Marek Ząbkowski, Tomasz Zdanowski, Robert Brytan, Marek Patera, Janusz Nowak, Zbigniew Kade, Grzegorz Wańkowicz, Zofia Med Sci Monit Animal Study BACKGROUND: The pathomechanism of acute hepatorenal syndrome (HRS), a particular form of acute renal failure that occurs in the course of acute liver injury, is still poorly understood. The aim of our study was to estimate the influence of the activation and inhibition of the nitric oxide pathway on the water/sodium balance and development of acute renal failure in the course of HRS. MATERIAL/METHODS: We used male Sprague-Dawley rats in the acute galactosamine (Ga1N) model of HRS. The nitric oxide synthase (NOS) inhibitors L-NAME and L-arginine were administered intraperitoneally before and after liver damage. RESULTS: HRS developed in all tested groups. L-NAME increased osmotic clearance and urine volume more effectively before liver injury. Furthermore, administration of L-NAME increased creatinine clearance both before and after Ga1N injection. A double dose of L-NAME did not yield further improvement before Ga1N injection, but improved creatinine clearance after Ga1N intoxication. Injection of L-arginine increased sodium excretion and urine volume, but only after liver injury. Moreover, L-arginine injected after Ga1N caused significant improvement of the creatinine clearance in a dose-dependent manner. CONCLUSIONS: Our study shows that inhibition of the nitric oxide pathway improves parameters of water and sodium balance and prevents development of acute renal failure in the course of acute liver injury and liver failure. Activation of the nitric oxide system also has a favorable influence on water/sodium balance and renal failure, but only after liver injury. International Scientific Literature, Inc. 2014-09-27 /pmc/articles/PMC4186324/ /pubmed/25270512 http://dx.doi.org/10.12659/MSM.890757 Text en © Med Sci Monit, 2014 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
spellingShingle Animal Study
Saracyn, Marek
Ząbkowski, Tomasz
Zdanowski, Robert
Brytan, Marek
Patera, Janusz
Nowak, Zbigniew
Kade, Grzegorz
Wańkowicz, Zofia
Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure
title Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure
title_full Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure
title_fullStr Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure
title_full_unstemmed Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure
title_short Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure
title_sort effect of nitric oxide pathway regulation on water/sodium balance and renal function in a rodent model of acute liver and renal failure
topic Animal Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186324/
https://www.ncbi.nlm.nih.gov/pubmed/25270512
http://dx.doi.org/10.12659/MSM.890757
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