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Department of Neurological Surgery, University of Washington School of Medicine, Seattle, Washington 98104
The purpose of this study was to investigate the
receptor subtypes that mediate the dilation of rat intracerebral
arterioles elicited by adenosine. Penetrating arterioles were isolated
from the rat brain, cannulated with the use of a micropipette system, and luminally pressurized to 60 mmHg. Both adenosine and the
A2A receptor-selective agonist CGS-21680 induced
dose-dependent vasodilation (
logEC50: 6.5 ± 0.2 and
8.6 ± 0.3, respectively). However, adenosine, which is capable of
activating both A2A and A2B receptors, caused a
greater maximal dilation than CGS-21680. The A2A
receptor-selective antagonist ZM-241385 (0.1 µM) only partially
inhibited the dilation induced by adenosine but almost completely
blocked CGS-21680-induced dilation. Neither
8-cyclopentyl-1,3-dipropylxanthine (0.1 µM), an A1
receptor-selective antagonist, nor MRS-1191 (0.1 µM), an A3 receptor-selective antagonist, attenuated adenosine dose
responses. Moreover, ZM-241385 had no effect on the dilation induced by
ATP (10 µM) or acidic (pH 6.8) buffer. We concluded that the
A2A receptor subtype mediates adenosine-induced dilation of
intracerebral arterioles in the rat brain. Furthermore, our results
suggest that A2B receptors may also participate in the
dilation response to adenosine.
cerebral blood flow; parenchymal arteriole; CGS-21680; ZM-241385; adenosine receptors
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