Argininstoffwechsel im hypertrophischen und hyperplastischen Nierengewebe und im Myokard bei Arbeitshypertrophie des Herzens infolge renalen Hochdruckes

Bogatzki, Marianne

doi:10.1007/bf02045500

Cited by 2 publications

(2 citation statements)

References 21 publications

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“…Erbas et al showed that administration of N-acetylcysteine normalizes arginase activity in the kidney and improved the situation following ischemia and reperfusion (Erbas et al, 2004 ). Noteworthy, carefully measurements of renal arginase activity 2 weeks after the insult have revealed an up-regulation of the enzyme in the kidney that is required for the proliferative repair of the damaged kidney (Bogatzki, 1963 ). As in the kidney, ROS in the presence of high NOS activity trigger neurological disorders to hypoxia/anoxia in brain and improving arginase activity is again associated with protection (Swamy et al, 2010 ).…”

Section: Arginase Activation In Non-cardiac Tissuesmentioning

confidence: 99%

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

2015

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Induction and activation of arginase is among the fastest responses of the heart to ischemic events. Induction of arginase expression and enzyme activation under ischemic conditions shifts arginine consumption from nitric oxide formation (NO) to the formation of ornithine and urea. In the heart such a switch in substrate utilization reduces the impact of the NO/cGMP-pathway on cardiac function that requires intact electromechanical coupling but at the same time it induces ornithine-dependent pathways such as the polyamine metabolism. Both effects significantly reduce the recovery of heart function during reperfusion and thereby limits the success of reperfusion strategies. In this context, changes in arginine consumption trigger cardiac remodeling in an unfavorable way and increases the risk of arrhythmia, specifically in the initial post-ischemic period in which arginase activity is dominating. However, during the entire ischemic period arginase activation might be a meaningful adaptation that is specifically relevant for reperfusion following prolonged ischemic periods. Therefore, a precise understanding about the underlying mechanism that leads to arginase induction as well as of it's mechanistic impact on post-ischemic hearts is required for optimizing reperfusion strategies. In this review we will summarize our current understanding of these processes and give an outlook about possible treatment options for the future.

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Section: Arginase Activation In Non-cardiac Tissuesmentioning

confidence: 99%

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

2015

View full text Add to dashboard Cite

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“…Erbas et al showed that administration of N-acetylcysteine normalizes arginase activity in the kidney and improved the situation following ischemia and reperfusion (Erbas et al, 2004). Noteworthy, carefully measurements of renal arginase activity 2 weeks after the insult have revealed an up-regulation of the enzyme in the kidney that is required for the proliferative repair of the damaged kidney (Bogatzki, 1963). As in the kidney, ROS in the presence of high NOS activity trigger neurological disorders to hypoxia/anoxia in brain and improving arginase activity is again associated with protection (Swamy et al, 2010).…”

Section: Arginase Activation In Non-cardiac Tissuesmentioning

confidence: 99%

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

2015

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Arginase Isoforms and Biological Activity Arginase is an enzyme that catalyzes the hydrolysis of L-arginine into urea and ornithine. It is expressed in two different isoforms. Arginase I is located in the cytosol and well-known from hepatic metabolism in which arginase is responsible for the elimination of metabolites from amino acid and nucleotide metabolism. The enzyme is expressed throughout the body in endothelial cells and muscle cells (Gonon et al., 2012). In contrast to arginase I, arginase II is predominantly located in the mitochondrial matrix and seems to be linked directly to polyamine metabolism, although its exact function is not known (Morris, 2005). The polyamine metabolism synthesizes polyamines such as spermine and spermidine that are required for cellular growth. The rate limiting step of this pathway is the induction of

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Argininstoffwechsel im hypertrophischen und hyperplastischen Nierengewebe und im Myokard bei Arbeitshypertrophie des Herzens infolge renalen Hochdruckes

Cited by 2 publications

References 21 publications

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

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