Adenosine and muscle vasodilatation in acute systemic hypoxia
Adenosine and muscle vasodilatation in acute systemic hypoxia
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DOI：
10.1046/j.1365-201x.2000.00709.x
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发表时间：
2000-04-01
期刊：
影响因子：
--
通讯作者：
Marshall, JM
中科院分区：
文献类型：
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作者：
Marshall, JM
当骨骼肌和心肌的代谢增加时，腺苷被释放出来：它通过引起血管舒张来耦合O-2供应和O-2需求。这篇综述认为，腺苷在骨骼肌系统性缺氧中起着类似的作用。它占肌肉血管传导性增加的大约50%，并且在肌肉内，它引起个体小动脉扩张，从而最大化O-2的分布，并且当O-2输送减少时允许O-2消耗保持恒定。体内和体外研究表明，腺苷可以通过几种不同的方式诱导扩张。这篇综述认为，在全身缺氧时，腺苷主要从内皮释放，并以一氧化氮（NO）依赖的方式作用于内皮A（1）受体，产生扩张。A（1）受体刺激通过ATP敏感性K+（K-ATP）通道开放启动的过程增加NO的合成。此外，最近的研究结果表明，野牡丹素也作出了重大贡献，缺氧引起的扩张，但腺苷，NO和野牡丹素的扩张途径是相互依赖的。此外，从骨骼肌纤维释放的腺苷通过刺激肌纤维上的A（1）和A（2）受体、打开K-ATP通道并允许K+流出（其为血管扩张剂）而间接有助于扩张。最后，通过作用于内皮A（1）受体，腺苷减弱交感神经活动的恒定或爆发模式的血管收缩作用。这限制了交感神经系统在全身性缺氧已经受损时减少向肌肉输送O-2的程度。
Adenosine is released by skeletal and cardiac muscles when their metabolism increases: it serves to couple O-2 supply with O-2 demand by causing vasodilatation. This review argues that adenosine plays a similar role in skeletal muscle in systemic hypoxia. It accounts for approximate to 50% of the increase in muscle vascular conductance and, within muscle, it causes dilatation of individual arterioles, thus maximizing the distribution of O-2 and allowing O-2 consumption to remain constant when O-2 delivery is reduced. In vivo and in vitro studies have indicated that adenosine can induce dilatation in several different ways. This review argues that during systemic hypoxia, adenosine is predominantly released from the endothelium and acts on endothelial A(1) receptors to produce dilatation in a nitric oxide (NO)-dependent manner. A(1) receptor stimulation increases the synthesis of NO by a process initiated by opening of ATP-sensitive K+ (K-ATP) channels. Moreover, recent findings suggest that prostaglandins also make a major contribution to the hypoxia-induced dilatation, but that the dilator pathways for adenosine, NO and prostaglandins are interdependent. In addition, adenosine released from the skeletal muscle fibres contributes indirectly to the dilatation by stimulating A(1) and A(2) receptors on the muscle fibres, opening K-ATP channels and allowing efflux of K+, which is a vasodilator. Finally, by acting on endothelial A(1) receptors, adenosine attenuates the vasoconstrictor effects of constant or bursting patterns of sympathetic activity. This limits the extent to which the sympathetic nervous system can reduce O-2 delivery to muscle when it is already compromized by systemic hypoxia.