Contribution of adenosine A2A and A2B receptors and heme oxygenase to AMPA-induced dilation of pial arterioles in rats.
Contribution of adenosine A2A and A2B receptors and heme oxygenase to AMPA-induced dilation of pial arterioles in rats.
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腺苷 A2A 和 A2B 受体以及血红素加氧酶对 AMPA 诱导的大鼠软脑膜小动脉扩张的贡献。
DOI：
10.1152/ajpregu.00757.2005
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Koehler,RaymondC
中科院分区：
文献类型：
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作者：
Ohata,Hiroto;Cao,Suyi;Koehler,RaymondC
Nitric oxide (NO) has been implicated in mediation of cerebral vasodilation during neuronal activation and, specifically, in pharmacological activation ofN-methyl-d-aspartate (NMDA) and kainate receptors. Possible mediators of cerebral vasodilation to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) have not been well studied in mature brain, although heme oxygenase (HO) activity has been implicated in newborn pigs. In anesthetized rats, 5 min of topical superfusion of 30 and 100 μM AMPA on the cortical surface through a closed cranial window resulted in increases in pial arteriolar diameter. The dilatory response to AMPA was not inhibited by superfusion of an NO synthase inhibitor, a cyclooxygenase-2 inhibitor, or a cytochromeP-450 epoxygenase inhibitor, all of which have been shown to inhibit the cortical blood flow response to sensory activation. However, the 48 ± 13% dilation to 100 μM AMPA was attenuated 56–71% by superfusion of the adenosine A2Areceptor antagonist ZM-241385, the A2Breceptor antagonist alloxazine, and the HO inhibitor chromium mesoporphyrin. Combination of the latter three inhibitors did not attenuate the dilator response more than the individual inhibitors, whereas an AMPA receptor antagonist fully blocked the vasodilation to AMPA. These results indicate that cortical pial arteriolar dilation to AMPA does not require activation of NO synthase, cyclooxygenase-2, or cytochromeP-450 epoxygenase but does depend on activation of adenosine A2Aand A2Breceptors. In addition, CO derived from HO appears to play a role in the vascular response to AMPA receptor activation in mature brain by a mechanism that is not additive with that of adenosine receptor activation.
