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Mechanism of contractile dysfunction induced by serotonin in coronary artery in spontaneously hypertensive rats.

5-羟色胺诱导自发性高血压大鼠冠状动脉收缩功能障碍的机制。

  • 影响因子:2.08
  • DOI:10.1007/s00210-020-01813-5
  • 作者列表:"Wang H","Gao XY","Rao F","Yang H","Wang ZY","Liu L","Kuang SJ","Wu Q","Deng CY","Xu JS
  • 发表时间:2020-01-24
Abstract

:Hypertension is one of the risk factors for coronary heart disease. The present study investigated the mechanism of contractile dysfunction induced by serotonin (5-HT) in coronary artery in spontaneously hypertensive rats (SHRs). Coronary arteries were isolated form SHRs and Wistar rats. Arterial ring contraction was measured using a multi myograph system. Intracellular calcium concentration was measured with a Ca2+ probe fluo-4/AM in vascular smooth muscle cells (VSMCs) isolated from coronary arteries. Signaling pathway-related proteins were assayed by western blotting. A 5-HT2A receptor blocker, sarpogrelate, completely eliminated coronary artery contraction induced by 5-HT. PLCβ inhibitor U73122 also significantly inhibited the response to 5-HT. Compared with the Wistar rats, serotonin (5-HT)- and CaCl2-induced coronary vasoconstriction in the SHRs was significantly reduced. Rho-associated protein kinase inhibitor Y27632, PKC inhibitor rottlerin, and L-type calcium channel blocker nifedipine inhibited the 5-HT-induced coronary artery contraction in a dose-dependent manner in SHRs and Wistar rats. However, the inhibitory effects were reduced in SHRs. In addition, store-operated Ca2+ (SOC) induced an obvious Ca2+ influx in coronary arterial smooth muscle cells, whereas SOC-mediated contraction was very slight in coronary arteries. At the same time, it was found that 5-HT2AR, IP3R, and Cav1.2 protein expression and PKCδ activity were decreased, and STIM1 and Orai1 were increased in VSMCs from coronary arteries of SHRs compared with Wistar rats. These results implicate calcium-handling dysfunction mediated by the 5-HT2A receptor and downstream signaling pathway might lead to a reduction in 5-HT-induced contraction in SHR coronary arteries.

摘要

: 高血压是冠心病的危险因素之一。本研究探讨 5-羟色胺 (5-HT) 引起自发性高血压大鼠 (shr) 冠状动脉收缩功能障碍的机制。从 SHRs 和 Wistar 大鼠中分离冠状动脉。使用多肌图系统测量动脉环收缩。用 Ca2 + 探针 fluo-4/AM 测定冠状动脉血管平滑肌细胞 (VSMCs) 内钙离子浓度。Western blotting 检测信号通路相关蛋白。一种 5-HT2A 受体阻断剂 sarpogere 完全消除了 5-HT 诱导的冠状动脉收缩。Plc β 抑制剂 U73122 也显著抑制对 5-HT 的反应。与 Wistar 大鼠相比,SHRs 的 5-羟色胺 (5-HT)-和 CaCl2-induced 冠状动脉收缩显著降低。Rho 相关蛋白激酶抑制剂 Y27632 、 PKC 抑制剂 rottlerin 和 L 型钙通道阻滞剂硝苯地平以剂量依赖性方式抑制 SHRs 和 Wistar 大鼠 5-ht 诱导的冠状动脉收缩。然而,SHRs 的抑制作用降低。此外,存储操作的 Ca2 + (SOC) 在冠状动脉平滑肌细胞中诱导了明显的 Ca2 + 内流,而 SOC 介导的收缩在冠状动脉中非常轻微。同时发现 5-HT2AR 、 IP3R 、和 Cav1.2 蛋白表达和 pkc δ 活性降低, 与 Wistar 大鼠相比,SHRs 冠状动脉 VSMCs 中 STIM1 和 Orai1 增加。这些结果暗示由 5-HT2A 受体和下游信号通路介导的钙处理功能障碍可能导致 SHR 冠状动脉 5-ht 诱导的收缩减少。

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