ATP protects, by way of receptor-mediated mechanisms, against hypoxia-induced injury in renal proximal tubules

Andreas Kribben; Thorsten Feldkamp; Markus Horbelt; Bettina Lange; Frank Pietruck; Stefan Herget-Rosenthal; Uwe Heemann; Thomas Philipp

doi:10.1067/mlc.2003.7

ATP protects, by way of receptor-mediated mechanisms, against hypoxia-induced injury in renal proximal tubules

Andreas Kribben, Thorsten Feldkamp, Markus Horbelt, Bettina Lange, Frank Pietruck, Stefan Herget-Rosenthal, Uwe Heemann, Thomas Philipp

Associate Professorship of Nephrology

University Hospital of Essen

Research output: Contribution to journal › Article › peer-review

17 Scopus citations

Abstract

We examined the effect of ATP on hypoxia-induced injury in freshly isolated rat renal proximal tubules and compared it with the effects of stable ATP analogues and ATP degradation products. Extracellular ATP significantly reduced hypoxia-induced structural cell damage (lactate dehydrogenase release). P₂-receptor agonistic ATP analogues, including 2′-methylthio-ATP (2-Me-S-ATP), were also protective. In contrast, the P₁-agonistic degradation products AMP and adenosine were not protective. Hypoxia-induced functional cell damage (loss of cellular potassium) was not changed by ATP or 2-Me-S-ATP. We therefore conclude that the protective property of ATP is not based on an effect of the degradation products or on a direct effect on cellular energy metabolism. The data indicate that the protective effect of ATP is mediated by P₂ receptors.

Original language	English
Pages (from-to)	67-73
Number of pages	7
Journal	Journal of Laboratory and Clinical Medicine
Volume	141
Issue number	1
DOIs	https://doi.org/10.1067/mlc.2003.7
State	Published - 1 Jan 2003

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title = "ATP protects, by way of receptor-mediated mechanisms, against hypoxia-induced injury in renal proximal tubules",

abstract = "We examined the effect of ATP on hypoxia-induced injury in freshly isolated rat renal proximal tubules and compared it with the effects of stable ATP analogues and ATP degradation products. Extracellular ATP significantly reduced hypoxia-induced structural cell damage (lactate dehydrogenase release). P2-receptor agonistic ATP analogues, including 2′-methylthio-ATP (2-Me-S-ATP), were also protective. In contrast, the P1-agonistic degradation products AMP and adenosine were not protective. Hypoxia-induced functional cell damage (loss of cellular potassium) was not changed by ATP or 2-Me-S-ATP. We therefore conclude that the protective property of ATP is not based on an effect of the degradation products or on a direct effect on cellular energy metabolism. The data indicate that the protective effect of ATP is mediated by P2 receptors.",

author = "Andreas Kribben and Thorsten Feldkamp and Markus Horbelt and Bettina Lange and Frank Pietruck and Stefan Herget-Rosenthal and Uwe Heemann and Thomas Philipp",

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T1 - ATP protects, by way of receptor-mediated mechanisms, against hypoxia-induced injury in renal proximal tubules

AU - Kribben, Andreas

AU - Feldkamp, Thorsten

AU - Horbelt, Markus

AU - Lange, Bettina

AU - Pietruck, Frank

AU - Herget-Rosenthal, Stefan

AU - Heemann, Uwe

AU - Philipp, Thomas

N1 - Funding Information: Supported by a grant from the Deutsche Forschungsgemeinschaft (Kr 1108/2-2) and by a grant from the IFORES program of the University Essen.

PY - 2003/1/1

Y1 - 2003/1/1

N2 - We examined the effect of ATP on hypoxia-induced injury in freshly isolated rat renal proximal tubules and compared it with the effects of stable ATP analogues and ATP degradation products. Extracellular ATP significantly reduced hypoxia-induced structural cell damage (lactate dehydrogenase release). P2-receptor agonistic ATP analogues, including 2′-methylthio-ATP (2-Me-S-ATP), were also protective. In contrast, the P1-agonistic degradation products AMP and adenosine were not protective. Hypoxia-induced functional cell damage (loss of cellular potassium) was not changed by ATP or 2-Me-S-ATP. We therefore conclude that the protective property of ATP is not based on an effect of the degradation products or on a direct effect on cellular energy metabolism. The data indicate that the protective effect of ATP is mediated by P2 receptors.

AB - We examined the effect of ATP on hypoxia-induced injury in freshly isolated rat renal proximal tubules and compared it with the effects of stable ATP analogues and ATP degradation products. Extracellular ATP significantly reduced hypoxia-induced structural cell damage (lactate dehydrogenase release). P2-receptor agonistic ATP analogues, including 2′-methylthio-ATP (2-Me-S-ATP), were also protective. In contrast, the P1-agonistic degradation products AMP and adenosine were not protective. Hypoxia-induced functional cell damage (loss of cellular potassium) was not changed by ATP or 2-Me-S-ATP. We therefore conclude that the protective property of ATP is not based on an effect of the degradation products or on a direct effect on cellular energy metabolism. The data indicate that the protective effect of ATP is mediated by P2 receptors.

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JF - Journal of Laboratory and Clinical Medicine

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ATP protects, by way of receptor-mediated mechanisms, against hypoxia-induced injury in renal proximal tubules

Abstract

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