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Vol. 291, Issue 3, 988-993, December 1999
Department of Pharmacology (A.N., Y.A., T.F., M.R., S.K., Y.A.) and
Research Equipment Center (A.M.), Kagawa Medical University, Miki-cho,
Kita-gun, Kagawa, Japan
Studies were carried out to determine the intrarenal adenosine
production during hypoxia, and the protective effects of a selective
adenosine A1 receptor antagonist
8-(noradamantan-3-yl)-1,3-dipropylxanthine (KW-3902) on hypoxia-induced
renal hemodynamic changes. We used an in vivo microdialysis method and
measured the renal interstitial concentration of adenosine in response
to hypoxic exposure in anesthetized mechanically ventilated rabbits.
Normocapnic systemic hypoxia (PaO2 = 32 ± 6 mm
Hg) caused a significant decrease in renal blood flow and increase in
renal vascular resistance, indicating a renal vasoconstriction. The
basal interstitial concentration of adenosine in the cortex was
293 ± 70 nM, which was significantly higher than that in the
medulla (170 ± 23 nM). Five minutes after beginning hypoxia, the
renal interstitial concentration of adenosine approximately tripled in
the cortex and doubled in the medulla. During treatment with KW-3902,
hypoxemia caused a similar increase in the adenosine concentration
compared with that in the absence of KW-3902. The administration of
KW-3902, however, significantly attenuated hypoxia-induced reduction in
renal blood flow. These results suggest that adenosine was involved in
hypoxia-induced renal vasoconstriction via its effects on adenosine
A1 receptors, and that KW-3902 had a partial protective
effect against renal vasoconstriction during hypoxemia.
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