HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine >
Peer-reviewed Journal Articles, etc >

Adenosine and inosine release during hypoxia in the isolated spinal cord of neonatal rats

Files in This Item:
BJP161-8_1806-1816.pdf311.06 kBPDFView/Open
Please use this identifier to cite or link to this item:

Title: Adenosine and inosine release during hypoxia in the isolated spinal cord of neonatal rats
Authors: Takahashi, T. Browse this author
Otsuguro, K. Browse this author →KAKEN DB
Ohta, T. Browse this author
Ito, S. Browse this author
Keywords: hypoxia
spinal cord
Issue Date: Dec-2010
Publisher: Blackwell Publishing
Journal Title: British Journal of Pharmacology
Volume: 161
Issue: 8
Start Page: 1806
End Page: 1816
Publisher DOI: 10.1111/j.1476-5381.2010.01002.x
Abstract: Background and purpose: Adenosine and inosine accumulate extracellularly during hypoxia/ischemia in the brain and may act as neuroprotectants. In spinal cord, there is pharmacological evidence for increases in extracellular adenosine during hypoxia, but no direct measurements of purine release, and furthermore the efflux pathways and origin of extracellular purines are unknown. To characterize hypoxia-evoked purine accumulation, we examined the effect of acute hypoxia on the extracellular levels of adenosine and inosine in the isolated rat spinal cord. Experimental approach: Extracellular adenosine and inosine concentrations were assayed in an in vitro preparation of the isolated spinal cord of the neonatal rat by high performance liquid chromatography (HPLC). Key results: The extracellular level of inosine was about tenfold higher than that of adenosine. Acute hypoxia (10 min) caused a temperature-dependent increase in these two purines, which was inhibited by an increase in external Ca2+, but not by several inhibitors of efflux pathways or metabolic enzymes of adenine nucleotides. Inhibitors of adenosine deaminase or the equilibrative nucleoside transporter (ENT) abolished the hypoxia-evoked increase in inosine but not adenosine. A glial metabolic inhibitor abolished the increase of both purines evoked by hypoxia but not by oxygen-glucose deprivation, hypercapnia or an adenosine kinase inhibitor. Conclusions and implications: Our data suggest that hypoxia releases adenosine itself from intracellular sources. Inosine formed intracellularly may be released through ENTs. During hypoxia, astrocytes appear to play a key role in purine release from the rat spinal cord.
Rights: The definitive version is available at
Type: article (author version)
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 乙黒 兼一

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 - Hokkaido University