Shiina T, Shimizu Y, Boudaka A, Wörl J, Takewaki T
Laboratory of Veterinary Physiology, Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Yanagido 1-1, Gifu 501-1193, Japan.
Neuroscience. 2006 May 12;139(2):495-503. doi: 10.1016/j.neuroscience.2005.12.027. Epub 2006 Feb 3.
The objective of the present study was to investigate the hypothesis of the presence of a local neural reflex modulating the vagally mediated contractions of striated muscle in the rat esophagus and to determine the possible involvement of tachykinins in such a local neural reflex. Electrical stimulation of the vagus nerve evoked twitch contractile responses that were abolished by d-tubocurarine (5 microM). Capsaicin (1-100 microM) inhibited the vagally mediated twitch contractions o f the normal rat esophageal preparations concentration-dependently but not those of the neonatally capsaicin-treated ones. NG-nitro-L-arginine methyl ester (100 microM), a nitric oxide synthase inhibitor, blocked the inhibitory effect of capsaicin and exogenous application of a nitric oxide donor (1 mM) inhibited the vagally mediated twitch contractions. Capsaicin suppressed acetylcholine release from the normal rat esophageal segments evoked by vagus nerve stimulation but not that from the neonatally capsaicin-treated ones. A selective tachykinin NK1 receptor antagonist (0.1 or 1 microM) attenuated the inhibitory effect of capsaicin. However, antagonists of tachykinin NK2, tachykinin NK3 and calcitonin gene-related peptide receptors (1 microM) did not have any effect. A tachykinin NK1 receptor agonist (1 or 5 microM) inhibited the vagally mediated twitch contractions, which was prevented by NG-nitro-L-arginine methyl ester (100 microM). These data suggest that the rat esophagus might have a local neural reflex inhibiting the vagally mediated striated muscle motility, which consists of capsaicin-sensitive sensory neurons and myenteric nitrergic neurons, and that tachykinins might be involved in the neural reflex through tachykinin NK1 receptors.
本研究的目的是探讨存在局部神经反射调节大鼠食管横纹肌迷走神经介导收缩的假说，并确定速激肽在这种局部神经反射中可能的参与情况。迷走神经电刺激诱发的抽搐收缩反应可被d -筒箭毒碱（5 microM）消除。辣椒素（1 - 100 microM）浓度依赖性地抑制正常大鼠食管标本中迷走神经介导的抽搐收缩，但对新生期用辣椒素处理过的标本则无此作用。一氧化氮合酶抑制剂NG -硝基 - L -精氨酸甲酯（100 microM）阻断了辣椒素的抑制作用，而外源性应用一氧化氮供体（1 mM）抑制了迷走神经介导的抽搐收缩。辣椒素抑制迷走神经刺激诱发的正常大鼠食管段乙酰胆碱释放，但对新生期用辣椒素处理过的食管段则无此作用。选择性速激肽NK1受体拮抗剂（0.1或1 microM）减弱了辣椒素的抑制作用。然而，速激肽NK2、速激肽NK3和降钙素基因相关肽受体的拮抗剂（1 microM）没有任何作用。速激肽NK1受体激动剂（1或5 microM）抑制了迷走神经介导的抽搐收缩，而NG -硝基 - L -精氨酸甲酯（100 microM）可阻止这种作用。这些数据表明，大鼠食管可能存在一种局部神经反射，抑制迷走神经介导的横纹肌运动，该反射由辣椒素敏感的感觉神经元和肌间一氧化氮能神经元组成，并且速激肽可能通过速激肽NK1受体参与该神经反射。
