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

被引：15

作者：

Kribben, A

Feldkamp, T

Hörbelt, M

Lange, B

Pietruck, F

Herget-Rosenthal, S

Heemann, U

Phillipp, T

机构：

[1] Klinik für Nieren- und H., Universitätsklinkum Essen, D-45122 Essen

来源：

JOURNAL OF LABORATORY AND CLINICAL MEDICINE | 2003年 / 141卷 / 01期

关键词：

D O I：

10.1067/mlc.2003.7

中图分类号：

R446 [实验室诊断]; R-33 [实验医学、医学实验];

学科分类号：

1001 ;

摘要：

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.

引用

页码：67 / 73

页数：7

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