Influence of endogenous neuropeptide Y (NPY) on the sympathetic-parasympathetic interaction in the canine heart
Influence of endogenous neuropeptide Y (NPY) on the sympathetic-parasympathetic interaction in the canine heart
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DOI：
10.1097/01.fjc.0000177986.21929.d8
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发表时间：
2005-10-01
影响因子：
3
通讯作者：
Nordlander, M
中科院分区：
文献类型：
--
作者：
Ilebekk, A;Björkman, JA;Nordlander, M
本研究的目的是通过神经肽 Y (NPY) 的释放及其对迷走神经和交感神经纤维上 NPY Y-2 受体的作用来检查交感-副交感神经相互作用对心率的影响。在对各种制剂和各种器官的其他研究中，实际上已通过 NPY Y-2 受体的激活证明了递质释放的减弱。然而，在目前对麻醉狗的研究中，我们首次检查了在强烈的心脏交感神经刺激期间释放的内源性 NPY 是否可以减弱迷走神经心动过缓。此外，我们还探讨了在适度的交感神经刺激过程中，交感神经递质的释放和心率是否会通过该受体系统受到影响。通过在施用其特异性受体拮抗剂BIIE0246之前和之后进行实验，揭示了NPY Y-2受体的重要性。我们发现，迷走神经刺激期间心动过缓的减弱被 BlIE0246 剂量依赖性地抵消，并且交感神经刺激引起的心动过速在 NPY Y2 受体阻断后仍然不受影响。因此，内源性 NPY 似乎通过刺激心脏迷走神经末梢上的交界前 NPY Y-2 受体来减弱迷走神经心动过缓，并且通过心脏交感神经纤维上的反馈回路来减弱递质释放和心动过速，但效率较低。
The purpose of this study was to examine the sympathetic-parasympathetic interactions on heart rate through release of neuropeptide Y (NPY) and its action on prejunctional NPY Y-2 receptors on vagal and sympathetic nerve fibers. In other studies on various preparations and in various organs, attenuation of transmitter release has in fact been demonstrated through activation of the NPY Y-2 receptor. In the present study on anesthetized dogs we examine, however, for the first time if vagal bradycardia is attenuated by endogenous NPY released during intense cardiac sympathetic stimulation. In addition, we explore if sympathetic transmitter release and heart rate, during moderate sympathetic stimulation, are affected through this receptor system. The significance of the NPY Y-2 receptor was revealed by performing experiments before and after administration of its specific receptor antagonist BIIE0246. We found that attenuation of the bradycardia during vagal nerve stimulation was dose-dependently counteracted by BlIE0246 and that the tachycardia elicited by sympathetic stimulation remained unaffected after NPY Y2 receptor blockade. Thus, endogenous NPY appears to attenuate vagal bradycardia by stimulating prejunctional NPY Y-2 receptors on cardiac vagal nerve terminals and, less efficiently, to attenuate transmitter release and tachycardia through a feedback loop on the cardiac sympathetic nerve fibers.