期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 284, 期 5, 页码 H1631-H1637出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00909.2002
关键词
theophylline; 4-{2-[7-amino-2-(2-furyl)(1,2,4)triazolo(2,3-a)-(1,3,5)triazin-5-ylamino]ethyl}phenol; cerebral blood flow
资金
- NINDS NIH HHS [NS 21076] Funding Source: Medline
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 muM glutamate and 100 muM N-methyl-D-aspartate (NMDA) dilated pial arterioles (baseline diameter 25 +/- 2 mum) by 17 +/- 1% and 18 +/- 4%, respectively. Coapplication of the nonselective Ado receptor antagonist theophylline ( Theo; 10 muM) significantly reduced glutamate- and NMDA-induced vasodilation to 4 +/- 2% (P < 0.01) and 6 ± 2% (P < 0.05), whereas the Ado A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (0.1 muM) had no effect. Moreover, application of the Ado A(2A) receptor-selective antagonist 4-{2-[7-amino-2-(2-furyl)(1,2,4)triazolo(2,3-a)(1,3,5)triazin-5-ylamino]ethyl}phenol (ZM-241385), either by superfusion (0.1 muM, 1 muM) or intravenously (1 mg/kg), significantly inhibited the pial arteriole dilation response to glutamate. Neither Theo nor ZM-241385 affected vascular reactivity to mild 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 A(2A) receptor subtype may be involved in this dilation response.
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