Pressor and tachycardic responses to intrathecal administration of neuropeptide FF in anesthetized rats
Pressor and tachycardic responses to intrathecal administration of neuropeptide FF in anesthetized rats
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麻醉大鼠鞘内注射神经肽 FF 的升压和心动过速反应
DOI：
10.1016/j.peptides.2009.11.003
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发表时间：
2010-04-01
期刊：
影响因子：
3
通讯作者：
Wang, Rui
中科院分区：
文献类型：
--
作者：
Fang, Quan;Li, Ning;Wang, Rui
神经肽 FF (NPFF) 属于神经肽家族，包括两个前体（pro-NPFFA 和 pro-NPFFB）和两个受体（NPFF1 和 NPFF2）。据报道，NPFF 和 NPFF 受体 mRNA 在大鼠和人脊髓中高度表达并定位。在本研究中，i.t.使用 NPFF 和两种相关激动剂 NPVF 和 dNPA 检查了 NPFF 系统对血压和心率的作用，这两种激动剂分别对 NPFF1 和 NPFF2 受体表现出最高的选择性。在氨基甲酸乙酯麻醉的大鼠中，NPFF 和相关肽（5-40 nmol，i.t.）在脊髓水平产生显着的升压和心动过速反应。这些作用是剂量依赖性的，并且三种肽的时间进程相似。此外，注射选择性 NPFF 拮抗剂 RF9 (20 nmol) 可以显着拮抗 20 nmol NPFF 和相关肽 (i.t.) 的心血管反应。此外，用α-肾上腺素受体拮抗剂酚妥拉明（1 mg/kg，静脉注射）预处理大鼠可显着降低 NPFF 的升压作用。然而，用毒蕈碱受体和肾上腺素受体拮抗剂（静脉注射）进行预处理可以阻止 NPFF 引起的心动过速效应。总的来说，我们的结果表明它。施用 NPFF 和相关肽可增加 MAP 和 HR，这可能是通过激活大鼠脊髓中的 NPFF 和 NPFF2 受体介导的。此外，我们的结果表明，毒蕈碱受体和肾上腺素受体参与了对 i.t 的心动过速反应。 NPFF,而α-肾上腺素受体在NPFF的升压作用调节中发挥重要作用。 (C) 2009 Elsevier Inc. 保留所有权利。
Neuropeptide FF (NPFF) belongs to a neuropeptide family including two precursors (pro-NPFFA and pro-NPFFB) and two receptors (NPFF1 and NPFF2). NPFF and NPFF receptor mRNAs have been reported to be highly expressed and localized in the rat and human spinal cord. In the present study, the i.t. action of NPFF system on blood pressure and heart rate were examined using NPFF and two related agonists, NPVF and dNPA, which exhibit highest selectivities for NPFF1 and NPFF2 receptors, respectively. In urethane-anesthetized rats, NPFF and related peptides (5-40 nmol, i.t.) produced significant pressor and tachycardic responses at the spinal cord level. These effects were dose-dependent and similar with respect to time-course for the three peptides. Furthermore, i.t, injection of RF9 (20 nmol), a selective NPFF antagonist, significantly antagonized the cardiovascular responses to 20 nmol NPFF and related peptides (i.t.). Moreover, pretreatment of the rats with alpha-adrenoceptor antagonist phentolamine (1 mg/kg, iv.) significantly reduced the pressor effects of NPFF. Nevertheless, pretreatment with muscarinic receptor and adrenoceptor antagonists (i.v.) could block the tachycardic effects induced by NPFF. Collectively, our results suggested that i.t. administration of NPFF and related peptides increased MAP and HR which were possibly mediated by the activation of both NPFF, and NPFF2 receptors in the rat spinal cord. In addition, our results showed that the muscarinic receptor and adrenoceptor participated in the tachycardic response to i.t. NPFF, while a-adrenoceptor played an important role in the regulation of pressor effect of NPFF. (C) 2009 Elsevier Inc. All rights reserved.