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Department of Neurological Surgery, University of Washington School of Medicine, Seattle, Washington 98104
In the present study, we
report the effects of adenosine receptor antagonists on pial
vasodilatation during contralateral sciatic nerve stimulation (SNS).
The pial circulation was observed through a closed cranial window in
-chloralose-anesthetized rats. In artificial cerebrospinal fluid
(CSF), SNS resulted in a 30.5 ± 13.2% increase in pial
arteriolar diameter in the hindlimb somatosensory cortex. Systemic
administration of the selective adenosine A2A receptor
antagonist,
4-(2-{7-amino-2-[2-furyl][3,2,4]triazolol[2,3-a][1,3,5]triazin-5-yl-amino} ethyl)phenol (ZM-241385), significantly (P < 0.05, n = 6) attenuated the SNS-induced vasodilatation.
Systemic administration of 8-(p-sulfophenyl)theophylline (8SPT), a nonselective antagonist that is blood-brain barrier (BBB)
impermeable, had no effect on vasodilatation to SNS. In contrast,
systemic theophylline, which readily penetrates the BBB, nearly
abolished the SNS-induced vasodilatation (P < 0.01; n = 7). Topical superfusion of 8SPT significantly
(P < 0.01; n = 6) attenuated
vasodilatation during SNS. Topical superfusion of 8- cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist, significantly potentiated
SNS-induced vasodilatation (P < 0.01;
n 
5). Hypercarbic vasodilatation and somatosensory-evoked potentials were not affected by any of the compounds tested. Our findings suggest that luminal endothelial adenosine receptors are not involved in the arteriolar response to SNS,
as demonstrated by a lack of effect with systemic 8SPT. Furthermore,
the adenosine A2A receptor subtype appears to be involved
in the dilator response to SNS. Finally, the neuromodulatory action of
adenosine, via the A1 receptor subtype, significantly influences SNS-induced vasodilatation. Thus the present study provides
further evidence for a role of adenosine in the regulation of CBF
during somatosensory stimulation.
ZM-241385; DPCPX; 8SPT; theophylline; EHNA; pial circulation; neuronal activity
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