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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >New insights on pyrimidine signalling within the arterial vasculature - Different roles for P2Y2 and P2Y6 receptors in large and small coronary arteries of the mouse
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New insights on pyrimidine signalling within the arterial vasculature - Different roles for P2Y2 and P2Y6 receptors in large and small coronary arteries of the mouse

机译：动脉血管内嘧啶信号传导的新见解-小鼠大，小冠状动脉中P2Y2和P2Y6受体的不同作用

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摘要

Extracellular pyrimidines activate P2Y receptors on both smooth muscle cells and endothelial cells, leading to vasoconstriction and relaxation respectively. The aim of this study was to utilize P2Y knock-out (KO) mice to determine which P2Y receptor subtype are responsible for the contraction and relaxation in the coronary circulation and to establish whether P2Y receptors have different functions along the mouse coronary vascular tree. We tested stable pyrimidine analogues on isolated coronary arteries from P2Y2 and P2Y6 receptor KO mice in a myograph setup. In larger diameter segments of the left descending coronary artery (LAD) (lumen diameter similar to 150 mu m) P2Y6 is the predominant contractile receptor for both UTP (uridine triphosphate) and UDP (uridine diphosphate) induced contraction. In contrast, P2Y2 receptors mediate endothelial-dependent relaxation. However, in smaller diameter LAD segments (lumen diameter similar to 50 mu m), the situation is opposite, with P2Y2 being the contractile receptor and P2Y6 functioning as a relaxant receptor along with P2Y2. Immunohistochemistry was used to confirm smooth muscle and endothelial localization of the receptors. In vivo measurements of blood pressure in WT mice revealed a biphasic response to the stable analogue UDP beta S. Based on the changes in P2Y receptor functionality along the mouse coronary arterial vasculature, we propose that UTP can act as a vasodilator downstream of its release, after being degraded to UDP, without affecting the contractile pyrimidine receptors. We also propose a model, showing physiological relevance for the changes in purinergic receptor functionality along the mouse coronary vascular tree. (C) 2016 Elsevier Ltd. All rights reserved.
机译：细胞外嘧啶激活平滑肌细胞和内皮细胞上的P2Y受体，分别导致血管收缩和松弛。这项研究的目的是利用P2Y敲除（KO）小鼠确定哪种P2Y受体亚型负责冠状动脉循环的收缩和松弛，并确定P2Y受体在小鼠冠状血管树上是否具有不同的功能。我们在肌电图设置中在来自P2Y2和P2Y6受体KO小鼠的分离冠状动脉上测试了稳定的嘧啶类似物。在左降冠状动脉（LAD）的较大直径段（管腔直径类似于150微米）中，P2Y6是UTP（三磷酸尿苷）和UDP（二磷酸尿苷）诱导的收缩的主要收缩受体。相反，P2Y2受体介导内皮依赖性舒张。但是，在较小直径的LAD片段（管腔直径类似于50μm）中，情况恰恰相反，P2Y2是收缩受体，P2Y6与P2Y2一起充当松弛受体。免疫组织化学用于确认受体的平滑肌和内皮定位。体内WT小鼠的血压测量显示出对稳定的类似物UDP beta S的双相反应。基于小鼠冠状动脉脉管系统中P2Y受体功能的变化，我们建议UTP可以在释放后充当血管舒张剂，降解为UDP后，不会影响可收缩的嘧啶受体。我们还提出了一个模型，该模型显示了沿小鼠冠状血管树的嘌呤能受体功能变化的生理相关性。 （C）2016 Elsevier Ltd.保留所有权利。

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