GLP-1 Relaxes Rat Coronary Arteries by Enhancing ATP-Sensitive Potassium Channel Currents.

Archives of internal medicine Pub Date : 2019-10-23 eCollection Date: 2019-01-01 DOI:10.1155/2019/1968785

Qian-Feng Xiong, Shao-Hua Fan, Xue-Wen Li, Yu Niu, Jing Wang, Xin Zhang, Yi-Fan Chen, Ya-Wei Shi, Li-Hui Zhang

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Abstract

GLP-1 is a new type of antidiabetic agent that possesses many beneficial effects. Although its cardiovascular actions have been widely examined, little is known about GLP-1's effects on the rat coronary artery (RCA) or about the mechanisms underpinning these effects. Here, we report that GLP-1 inhibits depolarization- or thromboxane receptor agonist (U46619)-induced RCA contraction in a dosage-dependent manner. Vasorelaxation was attenuated by denuding the endothelium, L-NAME (nitric oxide synthase inhibitor), and glyburide (K_ATP channel blocker) but was not affected by indomethacin (cyclooxygenase inhibitor), iberiotoxin [Ca²⁺-activated K⁺ channel (K_Ca) blocker], or 4-aminopyridine (K_V channel blocker). Furthermore, GLP-1 increased outward K⁺ currents by enhancing the K_ATP channel in rat coronary arterial smooth muscle cells (RCASMCs). These results show that GLP-1 is an endothelial-dependent vasospasmolytic agent in the RCA and imply that the relaxant effect is regulated by enhancing K_ATP rather than K_V or K_Ca currents in RCASMCs.

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GLP-1 通过增强 ATP 敏感性钾通道电流舒张大鼠冠状动脉

GLP-1 是一种新型的抗糖尿病药物，具有许多有益的作用。尽管其心血管作用已被广泛研究，但人们对 GLP-1 对大鼠冠状动脉（RCA）的影响或这些影响的机制知之甚少。在这里，我们报告了 GLP-1 以剂量依赖的方式抑制去极化或血栓素受体激动剂（U46619）诱导的 RCA 收缩。剥脱内皮、L-NAME（一氧化氮合酶抑制剂）和甘布肽（KATP 通道阻滞剂）均可减弱血管舒张，但吲哚美辛（环氧化酶抑制剂）、伊比妥辛[Ca2+激活的 K+ 通道（KCa）阻滞剂]或 4-氨基吡啶（KV 通道阻滞剂）均不影响血管舒张。此外，GLP-1 还通过增强大鼠冠状动脉平滑肌细胞（RCASMCs）的 KATP 通道来增加外向 K+ 电流。这些结果表明，GLP-1 是一种依赖于内皮的 RCA 血管痉挛溶解剂，并暗示其松弛作用是通过增强 RCASMCs 中的 KATP 而不是 KV 或 KCa 电流来调节的。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Archives of internal medicine 医学-医学：内科

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