The effects of NO synthesis inhibition on the uptake of endogenous nucleosides into the rat brain

Brain uptake of 3H endogenous nucleosides in rats was measured by Brain Uptake Index method, using 14C‐sucrose as a referent molecule. The values obtained in control group were 4.68±0.93 for adenosine, 4.10±0.72 for guanosine and 1.14±0.72 for thymidine, indicating significant blood‐to‐brain transpo...

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Bibliographic Details
Published in:Neuroscience research communications 1998-01, Vol.22 (1), p.11-20
Main Authors: Redzic, Zoran B., Gasic, Jovana M., Markovic, Ivanka D., Vojvodic, Vanesa P., Vranic, Valentina P., Jovanovic, Suzana S., Rakic, Ljubisa M.
Format: Article
Language:English
Subjects:
brain uptake
diphenyletiodonium
endogenous nucleosides
L-ω-nitro arginine methyl ester (L-NAME)
NO synthesis inhibition
rat
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Summary:Brain uptake of 3H endogenous nucleosides in rats was measured by Brain Uptake Index method, using 14C‐sucrose as a referent molecule. The values obtained in control group were 4.68±0.93 for adenosine, 4.10±0.72 for guanosine and 1.14±0.72 for thymidine, indicating significant blood‐to‐brain transport of purine nucleosides. NO‐synthase inhibition was induced by i.p. application of 25 mg/kg 1‐ω‐nitro‐arginin methyl ester (L‐NAME) and 5mg/kg diphenylethiodonium (brain parenchyma NOS inhibitor). HPLC analysis showed that the concentration of L‐NAME in brain was sufficient to cause inhibition of NOS. Application of L‐NAME resulted in significant inhibition of brain uptake for both purine nucleosides. Unlike adenosine, in the case of guanosine a correlation between the rate of brain uptake inhibition and the L‐NAME concentration in plasma, but not in brain, was obtained. Application of diphenylethiodonium also caused a significant decrease in both guanosine and adenosine brain uptake. The obtained results were not significantly different from the BUI values obtained after preapllication of L‐NAME. Our results suggest that NOS inhibition decreases brain uptake of purine nucleosides. Such effect(s) are probably due to the inhibition of brain parenchyma NOS.
ISSN:0893-6609
1520-6769
DOI:10.1002/(SICI)1520-6769(199801/02)22:1<11::AID-NRC3>3.0.CO;2-V