Role of adenosine and its receptors in the vasodilatation induced in the cerebral cortex of the rat by systemic hypoxia
Role of adenosine and its receptors in the vasodilatation induced in the cerebral cortex of the rat by systemic hypoxia
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DOI：
10.1111/j.1469-7793.1998.507bn.x
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发表时间：
1998-06-01
影响因子：
5.5
通讯作者：
Marshall, JM
中科院分区：
文献类型：
--
作者：
Coney, AM;Marshall, JM
1. 在麻醉大鼠中，我们检查了腺苷在全身缺氧（呼吸 8% O-2）引起的大脑皮层血管舒张中的作用。通过激光多普勒探头记录暴露的顶叶皮层 (CoRCF) 表面的红细胞流量，皮层血管电导 (CoVC) 计算为 CoRCF 除以平均动脉血压。 All agonists and antagonists were applied topically to the cortex.2. Systemic hypoxia or adenosine application for 5 or 10 min, respectively, induced an increase in CoRCF and CoVC. 8-苯茶碱 (8-PT) 显着降低了这些反应，8-苯茶碱 (8-PT) 是一种腺苷受体拮抗剂，在腺苷 A 和 A(2A) 受体亚型之间具有非选择性。相比之下，腺苷受体拮抗剂8-磺基苯茶碱（8-SPT）同样是非选择性的，但与8-PT不同的是，它不会穿过血脑屏障，可以减少腺苷诱导的CoRCF和CoVC的增加，但对缺氧诱导的CoRCF和CoVC的增加没有影响。3。 The A(2A) receptor agonist CGS21680 produced a substantial increase in CoRCF and CoVC, but the A(1) receptor agonist 2-chloro-N-6-cyclopentyladenosine had minimal effects.4. A(2A)受体拮抗剂ZM241385可减少腺苷诱导的CoRCF和CoVC的增加，并减少缺氧诱导的CoRCF的增加。5．我们提出，局部应用于大脑皮层的外源性腺苷通过作用于血管平滑肌上的 A(2A) 受体而产生血管舒张作用。然而，在全身缺氧期间，我们认为腺苷从内皮细胞中释放出来，作用于内皮A(2A)受体，从而产生缺氧引起的大脑皮层扩张的主要部分。
1. In anaesthetized rats, we have examined the role of adenosine in vasodilatation evoked in the cerebral cortex by systemic hypoxia (breathing 8% O-2). Red cell flux was recorded from the surface of the exposed parietal cortex (CoRCF) by a laser Doppler probe, cortical vascular conductance (CoVC) being computed as CoRCF divided by mean arterial blood pressure. All agonists and antagonists were applied topically to the cortex.2. Systemic hypoxia or adenosine application for 5 or 10 min, respectively, induced an increase in CoRCF and CoVC. These responses were substantially reduced by 8-phenyltheophylline (8-PT), an adenosine receptor antagonist which is non-selective between the adenosine A, and A(2A) receptor subtypes. By contrast, the adenosine receptor antagonist 8-sulphophenyltheophylline (8-SPT) which is similarly non-selective, but unlike 8-PT, does not cross the blood-brain barrier, reduced the increases in CoRCF and CoVC induced by adenosine, but had no effect on those induced by hypoxia.3. The A(2A) receptor agonist CGS21680 produced a substantial increase in CoRCF and CoVC, but the A(1) receptor agonist 2-chloro-N-6-cyclopentyladenosine had minimal effects.4. The A(2A) receptor antagonist ZM241385 reduced the increase in CoRCF and CoVC induced by adenosine and reduced the increase in CoRCF induced by hypoxia.5. We propose that exogenous adenosine that is topically applied to the cerebral cortex produces vasodilatation by acting on A(2A) receptors on the vascular smooth muscle. However, during systemic hypoxia, we propose that adenosine is released from endothelial cells and acts on endothelial A(2A) receptors to produce the major part of the hypoxia-induced dilatation in the cerebral cortex.