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Am J Physiol Heart Circ Physiol (January 23, 2003). doi:10.1152/ajpheart.00909.2002
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Submitted on October 21, 2002
Accepted on January 13, 2003

ADENOSINE RECEPTORS MEDIATE GLUTAMATE-EVOKED ARTERIOLAR DILATION IN THE RAT CEREBRAL CORTEX

Jeffrey J. Iliff1, Raimondo D'Ambrosio1, Al C. Ngai1*, and H R. Winn2

1 Department of Neurological Surgery, University of Washington, Seattle, WA, USA
2 Department of Biophysics and Physiology, University of Washington, Seattle, WA, USA

* To whom correspondence should be addressed. E-mail: ngai{at}u.washington.edu.

We tested the hypothesis that adenosine (ADO) mediates glutamate-induced vasodilation in the cerebral cortex, by monitoring pial arteriole diameter in chloralose-anesthetized rats equipped with closed cranial windows. Topical application of 100 µM glutamate and 100 µM N-methyl-D-aspartate (NMDA) dilated pial arterioles (baseline diameter 25 ± 2 µm) by 17 ± 1% and 18 ± 4%, respectively. Co-application of the non-selective ADO receptor antagonist theophylline (10 µM, THEO) significantly reduced glutamate- and NMDA-induced vasodilation to 4 ± 2% (p<.01) and 6 ± 2% (p<.05), whereas the ADO A1 receptor antagonist CPX (0.1 µM) had no effect. Moreover, application of the ADO A2A receptor-selective antagonist ZM-241385, either by superfusion (0.1 µM, 1 µM) or intravenously (1 mg/kg), significantly inhibited the pial arteriole dilation response to glutamate. Neither THEO nor ZM-241385 affected vascular reactivity to hypercapnia induced by 5% CO2 inhalation. These results suggest that ADO contributes to the dilation of rat cerebral arterioles induced by exogenous glutamate, and that the ADO A2A receptor subtype may be involved in this dilation response.




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