Burnstock G
Blood Vessels. 1987;24(3):156-60. doi: 10.1159/000158691.
Dual control of local blood flow by purines is described: adenosine 5'-triphosphate (ATP) released as a cotransmitter with noradrenaline from perivascular sympathetic nerves acts on P2X-purinoceptors on smooth muscle cells to produce vasoconstriction; ATP released from endothelial cells during hypoxia (and ADP released from aggregating platelets) acts on P2Y-purinoceptors on endothelial cells which results in production of endothelium-derived relaxing factor and subsequent vasodilatation. It is suggested that the endothelial-mediated vasodilatation is a pathophysiological mechanism to protect the host tissue (e.g. brain or heart) from damage produced by hypoxia following ischaemia. The ATP released from the endothelial cells is rapidly broken down to adenosine which augments this protective mechanism by acting directly on P1-purinoceptors on vascular smooth muscle to produce a longer lasting component of vasodilatation and on perivascular sympathetic nerve terminals to inhibit release of excitatory neurotransmitters. The possibility that impairment of normal endothelial-mediated responses in atherosclerosis and hypertension can lead to local vasospasm is considered.
作为与去甲肾上腺素共同递质从血管周围交感神经释放的5'-三磷酸腺苷（ATP）作用于平滑肌细胞上的P2X嘌呤受体，产生血管收缩；缺氧时内皮细胞释放的ATP（以及聚集血小板释放的ADP）作用于内皮细胞上的P2Y嘌呤受体，导致内皮衍生舒张因子的产生及随后的血管舒张。有人提出，内皮介导的血管舒张是一种病理生理机制，可保护宿主组织（如脑或心脏）免受缺血后缺氧产生的损伤。内皮细胞释放的ATP迅速分解为腺苷，腺苷通过直接作用于血管平滑肌上的P1嘌呤受体产生持久的血管舒张成分，并作用于血管周围交感神经末梢以抑制兴奋性神经递质的释放，从而增强这种保护机制。文中考虑了动脉粥样硬化和高血压中正常内皮介导反应受损可能导致局部血管痉挛的可能性。
