Smith-White Margaret A, Herzog Herbert, Potter Erica K
Prince of Wales Medical Research Institute, Prince of Wales Hospital, Barker St., Randwick 2031, Sydney, Australia.
Regul Pept. 2002 Feb 15;103(2-3):105-11. doi: 10.1016/s0167-0115(01)00368-8.
The aim of the study was to clarify the role of the Y(2) receptor in regulation of vagal control of the heart, using Y(2)((-/-)) receptor-knockout mice. Adult Y(2)((+/+),(-/-)) mice (50% C57BL/6-50% 129/SvJ background) were anaesthetised and artificially ventilated. Arterial blood pressure and pulse interval was recorded and both vagus nerves were cut. The cardiac end of the right vagus nerve was stimulated supra-maximally every 30 s (7 V, 2-2.5 Hz, 5 s). Neuropeptide Y (NPY) and a Y(2) receptor agonist, N-acetyl [Leu(28, 31)]NPY 24-36, were injected intravenously in both groups of mice. N-acetyl [Leu(28, 31)] NPY 24-36 was also administered to control mice in the presence of a Y(2) receptor antagonist, BIIE0246. Stimulation of the vagus nerve increased pulse interval (PI) by approximately 100 ms. NPY and N-acetyl [Leu(28, 31)] NPY 24-36 attenuated the increase in PI evoked by vagal stimulation in control mice only. The attenuation was reduced in the presence of BIIE0246. The results presented here show in Y(2)((-/-)) receptor-knockout mice that NPY and N-acetyl [Leu(28, 31)] NPY 24-36 have no effect on PI evoked by vagal stimulation. These findings demonstrate that NPY attenuates parasympathetic activity to the heart via the Y(2) receptor.
本研究旨在利用Y(2)(-/-)受体基因敲除小鼠阐明Y(2)受体在调节心脏迷走神经控制中的作用。成年Y(2)(+/+)、(-/-)小鼠（50% C57BL/6 - 50% 129/SvJ背景）经麻醉并进行人工通气。记录动脉血压和脉搏间期，双侧迷走神经切断。每隔30秒（7伏，2 - 2.5赫兹，5秒）以超强刺激右侧迷走神经的心脏端。两组小鼠均静脉注射神经肽Y（NPY）和Y(2)受体激动剂N - 乙酰[Leu(28, 31)]NPY 24 - 36。在存在Y(2)受体拮抗剂BIIE0246的情况下，也对对照小鼠给予N - 乙酰[Leu(28, 31)]NPY 24 - 36。刺激迷走神经使脉搏间期（PI）增加约100毫秒。仅在对照小鼠中，NPY和N - 乙酰[Leu(28, 31)]NPY 24 - 36减弱了迷走神经刺激引起的PI增加。在存在BIIE0246的情况下，这种减弱作用降低。此处呈现的结果表明，在Y(2)(-/-)受体基因敲除小鼠中，NPY和N - 乙酰[Leu(28, 31)]NPY 24 - 36对迷走神经刺激引起的PI无影响。这些发现证明，NPY通过Y(2)受体减弱心脏的副交感神经活动。
